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  • 101.
    Mousavi, Malahat
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB). Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Jonsson, Pär
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Kemiska institutionen.
    Antti, Henrik
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Kemiska institutionen.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nordin, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Bergdahl, Jan
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Institute of Clinical Dentistry, University of Tromsø, Tromsø, Norway.
    Eriksson, Kåre
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Moritz, Thomas
    Department of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences.
    Nilsson, Lars-Göran
    Umeå Center for Functional Brain Imaging, Umeå; Aging Research Center, Karolinska Institutet, Stockholm, Sweden.
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB). Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper. Umeå Center for Functional Brain Imaging, Umeå.
    Serum metabolomic biomarkers of dementia2014Ingår i: Dementia and geriatric cognitive disorders extra, E-ISSN 1664-5464, Vol. 4, nr 2, s. 252-62Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aims: This study compared serum metabolites of demented patients (Alzheimer's disease and vascular dementia) and controls, and explored serum metabolite profiles of nondemented individuals 5 years preceding the diagnosis. Methods: Cognitively healthy participants were followed up for 5-20 years. Cognitive assessment, serum sampling, and diagnosis were completed every 5 years. Multivariate analyses were conducted on the metabolite profiles generated by gas chromatography/time-of-flight mass spectrometry. Results: A significant group separation was found between demented patients and controls, and between incident cases and controls. Metabolites that contributed in both analyses were 3,4-dihydroxybutanoic acid, docosapentaenoic acid, and uric acid. Conclusions: Serum metabolite profiles are altered in demented patients, and detectable up to 5 years preceding the diagnosis. Blood sampling can make an important contribution to the early prediction of conversion to dementia.

  • 102. Mullins, Niamh
    et al.
    Bigdeli, Tim B.
    Borglum, Anders D.
    Coleman, Jonathan R., I
    Demontis, Ditte
    Mehta, Divya
    Power, Robert A.
    Ripke, Stephan
    Stahl, Eli A.
    Starnawska, Anna
    Anjorin, Adebayo
    Corvin, Aiden
    Sanders, Alan R.
    Forstner, Andreas J.
    Reif, Andreas
    Koller, Anna C.
    Swiatkowska, Beata
    Baune, Bernhard T.
    Mueller-Myhsok, Bertram
    Penninx, Brenda W. J. H.
    Pato, Carlos
    Zai, Clement
    Rujescu, Dan
    Hougaard, David M.
    Quested, Digby
    Levinson, Douglas F.
    Binder, Elisabeth B.
    Byrne, Enda M.
    Agerbo, Esben
    Streit, Fabian
    Mayoral, Fermin
    Bellivier, Frank
    Degenhardt, Franziska
    Breen, Gerome
    Marken, Gunnar
    Turecki, Gustavo
    Rouleau, Guy A.
    Grabe, Hans J.
    Voelzke, Henry
    Jones, Ian
    Giegling, Ina
    Agartz, Ingrid
    Melle, Ingrid
    Lawrence, Jacob
    Walters, James T. R.
    Strohmaier, Jana
    Shi, Jianxin
    Hauser, Joanna
    Biernacka, Joanna M.
    Vincent, John B.
    Kelsoe, John
    Strauss, John S.
    Lissowska, Jolanta
    Pimm, Jonathan
    Smoller, Jordan W.
    Guzman-Parra, Jose
    Berger, Klaus
    Scott, Laura J.
    Jones, Lisa A.
    Azevedo, M. Helena
    Trzaskowski, Maciej
    Kogevinas, Manolis
    Rietschel, Marcella
    Boks, Marco
    Ising, Marcus
    Grigoroiu-Serbanescu, Maria
    Hamshere, Marian L.
    Leboyer, Marion
    Frye, Mark
    Noethen, Markus M.
    Alda, Martin
    Preisig, Martin
    Nordentoft, Merete
    Boehnke, Michael
    O'Donovan, Michael C.
    Owen, Michael J.
    Pato, Michele T.
    Renteria, Miguel E.
    Budde, Monika
    Weissman, Myrna M.
    Wray, Naomi R.
    Bass, Nicholas
    Craddock, Nicholas
    Smeland, Olav B.
    Andreassen, Ole A.
    Mors, Ole
    Gejman, Pablo, V
    Sklar, Pamela
    McGrath, Patrick
    Hoffmann, Per
    McGuffin, Peter
    Lee, Phil H.
    Mortensen, Preben Bo
    Kahn, Rene S.
    Ophoff, Roel A.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Van Der Auwera, Sandra
    Djurovic, Srdjan
    Klaiber, Stefan
    Heilmann-Heimbach, Stefanie
    Jamain, Stephane
    Hamilton, Steven P.
    McElroy, Susan L.
    Lucae, Susanne
    Cichon, Sven
    Schulze, Thomas G.
    Hansen, Thomas
    Werge, Thomas
    Air, Tracy M.
    Nimgaonkar, Vishwajit
    Appadurai, Vivek
    Cahn, Wiepke
    Milaneschi, Yuri
    Fanous, Ayman H.
    Kendler, Kenneth S.
    McQuillin, Andrew
    Lewis, Cathryn M.
    GWAS of Suicide Attempt in Psychiatric Disorders and Association With Major Depression Polygenic Risk Scores2019Ingår i: American Journal of Psychiatry, ISSN 0002-953X, E-ISSN 1535-7228, Vol. 176, nr 8, s. 651-660Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: More than 90% of people who attempt suicide have a psychiatric diagnosis; however, twin and family studies suggest that the genetic etiology of suicide attempt is partially distinct from that of the psychiatric disorders themselves. The authors present the largest genome-wide association study (GWAS) on suicide attempt, using cohorts of individuals with major depressive disorder, bipolar disorder, and schizophrenia from the Psychiatric Genomics Consortium.

    Methods: The samples comprised 1,622 suicide attempters and 8,786 nonattempters with major depressive disorder; 3,264 attempters and 5,500 nonattempters with bipolar disorder; and 1,683 attempters and 2,946 nonattempters with schizophrenia. A GWAS on suicide attempt was performed by comparing attempters to nonattempters with each disorder, followed by a meta-analysis across disorders. Polygenic risk scoring was used to investigate the genetic relationship between suicide attempt and the psychiatric disorders.

    Results: Three genome-wide significant loci for suicide attempt were found: one associated with suicide attempt in major depressive disorder, one associated with suicide attempt in bipolar disorder, and one in the meta-analysis of suicide attempt in mood disorders. These associations were not replicated in independent mood disorder cohorts from the UK Biobank and iPSYCH. No significant associations were found in the meta-analysis of all three disorders. Polygenic risk scores for major depression were significantly associated with suicide attempt in major depressive disorder (R2=0.25%), bipolar disorder (R2=0.24%), and schizophrenia (R2=0.40%).

    Conclusions: This study provides new information on genetic associations and demonstrates that genetic liability for major depression increases risk for suicide attempt across psychiatric disorders. Further collaborative efforts to increase sample size may help to robustly identify genetic associations and provide biological insights into the etiology of suicide attempt.

  • 103. Musliner, Katherine L.
    et al.
    Mortensen, Preben B.
    McGrath, John J.
    Suppli, Nis P.
    Hougaard, David M.
    Bybjerg-Grauholm, Jonas
    Bækvad-Hansen, Marie
    Andreassen, Ole
    Pedersen, Carsten B.
    Pedersen, Marianne G.
    Mors, Ole
    Nordentoft, Merete
    Børglum, Anders D.
    Werge, Thomas
    Agerbo, Esben
    Nordin Adolfsson, Annelie (Medarbetare/bidragsgivare)
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Association of Polygenic Liabilities for Major Depression, Bipolar Disorder, and Schizophrenia With Risk for Depression in the Danish Population2019Ingår i: JAMA psychiatry, ISSN 2168-6238, E-ISSN 2168-622X, Vol. 76, nr 5, s. 516-525Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Importance: Although the usefulness of polygenic risk scores as a measure of genetic liability for major depression (MD) has been established, their association with depression in the general population remains relatively unexplored.

    Objective: To evaluate whether polygenic risk scores for MD, bipolar disorder (BD), and schizophrenia (SZ) are associated with depression in the general population and explore whether these polygenic liabilities are associated with heterogeneity in terms of age at onset and severity at the initial depression diagnosis.

    Design, Setting, and Participants: Participants were drawn from the Danish iPSYCH2012 case-cohort study, a representative sample drawn from the population of Denmark born between May 1, 1981, and December 31, 2005. The hazard of depression was estimated using Cox regressions modified to accommodate the case-cohort design. Case-only analyses were conducted using linear and multinomial regressions. The data analysis was conducted from February 2017 to June 2018.

    Exposures: Polygenic risk scores for MD, BD, and SZ trained using the most recent genome-wide association study results from the Psychiatric Genomics Consortium.

    Main Outcomes and Measures: The main outcome was first depressive episode (International Statistical Classification of Diseases and Related Health Problems, Tenth Revision [ICD-10] code F32) treated in hospital-based psychiatric care. Severity at the initial diagnosis was measured using the ICD-10 code severity specifications (mild, moderate, severe without psychosis, and severe with psychosis) and treatment setting (inpatient, outpatient, and emergency).

    Results: Of 34 573 participants aged 10 to 31 years at censoring, 68% of those with depression were female compared with 48.9% of participants without depression. Each SD increase in polygenic liability for MD, BD, and SZ was associated with 30% (hazard ratio [HR], 1.30; 95% CI, 1.27-1.33), 5% (HR, 1.05; 95% CI, 1.02-1.07), and 12% (HR, 1.12; 95% CI, 1.09-1.15) increases in the hazard of depression, respectively. Among cases, a higher polygenic liability for BD was associated with earlier depression onset (β = -.07; SE = .02; P = .002).

    Conclusions and Relevance: Polygenic liability for MD is associated with first depression in the general population, which supports the idea that these scores tap into an underlying liability for developing the disorder. The fact that polygenic risk for BD and polygenic risk for SZ also were associated with depression is consistent with prior evidence that these disorders share some common genetic overlap. Variations in polygenic liability may contribute slightly to heterogeneity in clinical presentation, but these associations appear minimal.

  • 104.
    Naghavi, Hamid Reza
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Lind, Johanna
    Department of Psychology, University of Oslo, Oslo, Norway.
    Nilsson, Lars-Göran
    Department of Psychology, Stockholm University, Stockholm, Sweden.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Fysiologi. Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Diagnostisk radiologi.
    Personality traits predict response to novel and familiar stimuli in the hippocampal region2009Ingår i: Psychiatry Research, ISSN 0165-1781, E-ISSN 1872-7123, Vol. 173, nr 2, s. 94-99Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Current evidence from genetic, neurochemical, and clinical research supports the notion that a combination of high novelty seeking and low harm avoidance traits (NS-ha) is reliably dissociable from the opposite personality profile (i.e., low novelty seeking and high harm avoidance, ns-HA). Little is known, however, about how the differences between these two types of personality are regulated by brain function. Here we used functional magnetic resonance imaging (fMRI) and recruited two groups of individuals, one group with the NS-ha profile and the other group with the ns-HA profile, to examine whether there is a difference between the two groups in their brain response to novel versus familiar word stimuli. Results revealed a differential pattern of response in an area in the hippocampal region, with the NS-ha group showing a greater sensitivity to novel stimuli and the ns-HA group demonstrating a greater response to familiar stimuli. We conclude that the response pattern to novel and familiar stimuli in the hippocampal region has a role in mediating differences between the NS-ha and ns-HA temperamental profiles.

  • 105. Nehme, Ralda
    et al.
    Zuccaro, Emanuela
    Ghosh, Sulagna Dia
    Li, Chenchen
    Sherwood, John L.
    Pietilainen, Olli
    Barrett, Lindy E.
    Limone, Francesco
    Worringer, Kathleen A.
    Kommineni, Sravya
    Zang, Ying
    Cacchiarelli, Davide
    Meissner, Alex
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Haggarty, Stephen
    Madison, Jon
    Muller, Matthias
    Arlotta, Paola
    Fu, Zhanyan
    Feng, Guoping
    Eggan, Kevin
    Combining NGN2 Programming with Developmental Patterning Generates Human Excitatory Neurons with NMDAR-Mediated Synaptic Transmission2018Ingår i: Cell reports, ISSN 2211-1247, E-ISSN 2211-1247, Vol. 23, nr 8, s. 2509-2523Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Transcription factor programming of pluripotent stem cells (PSCs) has emerged as an approach to generate human neurons for disease modeling. However, programming schemes produce a variety of cell types, and those neurons that are made often retain an immature phenotype, which limits their utility in modeling neuronal processes, including synaptic transmission. We report that combining NGN2 programming with SMAD and WNT inhibition generates human patterned induced neurons (hpiNs). Single-cell analyses showed that hpiN cultures contained cells along a developmental continuum, ranging from poorly differentiated neuronal progenitors to well-differentiated, excitatory glutamatergic neurons. The most differentiated neurons could be identified using a CAMK2A::GFP reporter gene and exhibited greater functionality, including NMDAR-mediated synaptic transmission. We conclude that utilizing single-cell and reporter gene approaches for selecting successfully programmed cells for study will greatly enhance the utility of hpiNs and other programmed neuronal populations in the modeling of nervous system disorders.

  • 106. Nilsson, Lars-Göran
    et al.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Bäckman, Lars
    de Frias, Cindy M
    Molander, Bo
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nyberg, Lars
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Betula: a prospective cohort study on memory, health and aging2004Ingår i: Aging, Neuropsychology and Cognition, ISSN 1382-5585, E-ISSN 1744-4128, Vol. 11, nr 2-3, s. 134-148Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    This article describes the Betula Study with respect to objectives, design, participants, and assessment instruments for health and cognition. Three waves of data collection have been completed in 5-year intervals since 1988-1990. A fourth wave started in 2003 and will be completed in 2005. An overview of Betula research is presented under the headings of memory and cognition and cognitive neuroscience. Health-related issues and sex differences as well as comparisons between cross-sectional and longitudinal studies are discussed in the first section. The influence of different genes and of some brain abnormalities for memory functioning in adulthood and old age constitute main topics in the second section. New data are presented on the association between blood pressure and dementia. We demonstrated that a demented group of participants had higher levels of systolic blood pressure and pulse pressure than non-dementia controls 10 years before diagnosis. The new fourth wave of data collection will, in addition to enriching the Betula database, permit revisiting and reanalyzing the existing data from new perspectives.

  • 107.
    Nordfjäll, Katarina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Svenson, Ulrika
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Norrback, Karl-Fredrik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Lenner, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Roos, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    The individual blood cell telomere attrition rate is telomere length dependent.2009Ingår i: PLoS genetics, ISSN 1553-7404, Vol. 5, nr 2, s. e1000375-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Age-associated telomere shortening is a well documented feature of peripheral blood cells in human population studies, but it is not known to what extent these data can be transferred to the individual level. Telomere length (TL) in two blood samples taken at approximately 10 years interval from 959 individuals was investigated using real-time PCR. TL was also measured in 13 families from a multigenerational cohort. As expected, we found an age-related decline in TL over time (r = -0.164, P<0.001, n = 959). However, approximately one-third of the individuals exhibited a stable or increased TL over a decade. The individual telomere attrition rate was inversely correlated with initial TL at a highly significant level (r = -0.752, P<0.001), indicating that the attrition rate was most pronounced in individuals with long telomeres at baseline. In accordance, the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age (r = -0.691, P<0.001). Abnormal blood TL has been reported at diagnosis of various malignancies, but in the present study there was no association between individual telomere attrition rate or prediagnostic TL and later tumor development. The collected data strongly suggest a TL maintenance mechanism acting in vivo, providing protection of short telomeres as previously demonstrated in vitro. Our findings might challenge the hypothesis that individual TL can predict possible life span or later tumor development.

  • 108.
    Nordfjäll, Katarina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Svenson, Ulrika
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Norrback, Karl-Fredrik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Roos, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Large-scale parent-child comparison confirms a strong paternal influence on telomere length2010Ingår i: European Journal of Human Genetics, ISSN 1018-4813, E-ISSN 1476-5438, Vol. 18, nr 3, s. 385-389Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Telomere length is documented to have a hereditary component, and both paternal and X-linked inheritance have been proposed. We investigated blood cell telomere length in 962 individuals with an age range between 0 and 102 years. Telomere length correlations were analyzed between parent-child pairs in different age groups and between grandparent-grandchild pairs. A highly significant correlation between the father's and the child's telomere length was observed (r=0.454, P<0.001), independent of the sex of the offspring (father-son: r=0.465, P<0.001; father-daughter: r=0.484, P<0.001). For mothers, the correlations were weaker (mother-child: r=0.148, P=0.098; mother-son: r=0.080, P=0.561; mother-daughter: r=0.297, P=0.013). A positive telomere length correlation was also observed for grandparent-grandchild pairs (r=0.272, P=0.013). Our findings indicate that fathers contribute significantly stronger to the telomere length of the offspring compared with mothers (P=0.012), but we cannot exclude a maternal influence on the daughter's telomeres. Interestingly, the father-child correlations diminished with increasing age (P=0.022), suggesting that nonheritable factors have an impact on telomere length dynamics during life.

  • 109. Nylander, P O
    et al.
    Drugge, U
    Holmgren, G
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLO-SL): a genealogical study of Swedish families of probable Finnish background.1996Ingår i: Clinical Genetics, ISSN 0009-9163, E-ISSN 1399-0004, Vol. 50, nr 5, s. 353-7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Four Swedish families in northern Sweden with polycystic lipomembranous osteodysplasia (PLO-SL) were studied genealogically. Historical and genealogical date provided evidence for a Finnish origin. Both parents of two of the families could be traced back to Finnish ancestors, and the other two families had a common origin in a region with a known Finnish influence, but without evidence for Finnish ancestry. PLO-SL is the first rare monogenic disease with an autosomal recessive inheritance in Sweden with a probable Finnish origin.

  • 110. Nylander, P O
    et al.
    Engström, C
    Chotai, Jayanti
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Wahlström, J
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Anticipation in Swedish families with bipolar affective disorder.1994Ingår i: Journal of Medical Genetics, ISSN 0022-2593, E-ISSN 1468-6244, Vol. 31, nr 9, s. 686-9Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Anticipation describes an inheritance pattern within a pedigree with an increase in disease severity or decrease in age at onset or both in successive generations. The phenomenon of anticipation has recently been shown to be correlated with the expansion of trinucleotide repeat sequences in different disorders. We have studied differences of age at onset and disease severity between two generations in 14 families with unilinear inheritance of bipolar affective disorder (BPAD). There was a significant difference in age at onset (p < 0.008), in episodes per year with (p < 0.006) and without (p < 0.03) lithium treatment, and in total episodes per year (p < 0.002) between generations I and II. Furthermore, there was a highly significant correlation (p < 0.001) in age at onset between generations I and II. No evidence for specific paternal or maternal inheritance was found. We found evidence of anticipation and could rule out ascertainment bias or some other artefact. Anticipation is thus an inheritance pattern in BPAD which suggests that the expansion of trinucleotide repeat sequences is a possible mode of inheritance in BPAD.

  • 111. Nylander, P O
    et al.
    Schlette, P
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Brändström, S
    Nilsson, M
    Forsgren, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Forsgren, L
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Migraine: temperament and character.1996Ingår i: Journal of Psychiatric Research, ISSN 0022-3956, E-ISSN 1879-1379, Vol. 30, nr 5, s. 359-68Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The personality profile of 26 adult migraine patients from a large Swedish family with migraine and 87 controls were studied by means of Cloninger's seven-factor model of Temperament and Character (TCI; Temperament and Character Inventory). For the diagnosis of migraine, a questionnaire, slightly modified to fit the criteria according to the AD HOC committee on the classification of headaches of the International Headache Society, was used. The TCI assesses four dimensions of temperament, including novelty-seeking (NS), harm avoidance (HA), reward dependence (RD) and persistence (P), and three dimensions of character, including self-directedness (SD), co-operativeness (C) and self-transcendence (ST). Psychiatric morbidity did not differ between this family and the general population. One migraine patient had double depression (dysthymia and recurrent depression) and one had a personality disorder. No significant difference could be found in the higher order dimensions of temperament (NS, HA, RD and P) and character (SD, C and ST) between migraine patients and controls. However, on the subscale level, NS showed a slightly higher average in NS1 (exploratory excitability) and a significantly higher (p = 0.0448) average in NS2 (impulsivity) in migraine patients compared to controls. Somatic anxiety has been shown to be positively correlated with NS, and especially impulsivity. Our results showed a tendency of this personality profile, and may suggest an association between migraine and somatic anxiety.

  • 112. O'Donovan, M C
    et al.
    Norton, N
    Williams, H
    Peirce, T
    Moskvina, V
    Nikolov, I
    Hamshere, M
    Carroll, L
    Georgieva, L
    Dwyer, S
    Holmans, P
    Marchini, J L
    Spencer, C C A
    Howie, B
    Leung, H-T
    Giegling, I
    Hartmann, A M
    Möller, H-J
    Morris, D W
    Shi, Y
    Feng, G
    Hoffmann, P
    Propping, P
    Vasilescu, C
    Maier, W
    Rietschel, M
    Zammit, S
    Schumacher, J
    Quinn, E M
    Schulze, T G
    Iwata, N
    Ikeda, M
    Darvasi, A
    Shifman, S
    He, L
    Duan, J
    Sanders, A R
    Levinson, D F
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Osby, U
    Terenius, L
    Jönsson, E G
    Cichon, S
    Nöthen, M M
    Gill, M
    Corvin, A P
    Rujescu, D
    Gejman, P V
    Kirov, G
    Craddock, N
    Williams, N M
    Owen, M J
    Analysis of 10 independent samples provides evidence for association between schizophrenia and a SNP flanking fibroblast growth factor receptor 22009Ingår i: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 14, nr 1, s. 30-36Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We and others have previously reported linkage to schizophrenia on chromosome 10q25-q26 but, to date, a susceptibility gene in the region has not been identified. We examined data from 3606 single-nucleotide polymorphisms (SNPs) mapping to 10q25-q26 that had been typed in a genome-wide association study (GWAS) of schizophrenia (479 UK cases/2937 controls). SNPs with P<0.01 (n=40) were genotyped in an additional 163 UK cases and those markers that remained nominally significant at P<0.01 (n=22) were genotyped in replication samples from Ireland, Germany and Bulgaria consisting of a total of 1664 cases with schizophrenia and 3541 controls. Only one SNP, rs17101921, was nominally significant after meta-analyses across the replication samples and this was genotyped in an additional six samples from the United States/Australia, Germany, China, Japan, Israel and Sweden (n=5142 cases/6561 controls). Across all replication samples, the allele at rs17101921 that was associated in the GWAS showed evidence for association independent of the original data (OR 1.17 (95% CI 1.06-1.29), P=0.0009). The SNP maps 85 kb from the nearest gene encoding fibroblast growth factor receptor 2 (FGFR2) making this a potential susceptibility gene for schizophrenia.

  • 113. Olofsson, Jonas K
    et al.
    Josefsson, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Enheten för demografi och åldrandeforskning (CEDAR).
    Ekström, Ingrid
    Wilson, Donald
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
    Nordin, Steven
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    Larsson, Maria
    Long-term episodic memory decline is associated with olfactory deficits only in carriers of ApoE-є42016Ingår i: Neuropsychologia, ISSN 0028-3932, E-ISSN 1873-3514, Vol. 85, s. 1-9Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The ɛ4 allele of the Apolipoprotein E gene is a genetic risk factor for late-onset dementia of the Alzheimers' type (DAT), which is characterized by loss of both episodic memory and olfactory functions. Little is known about the possible role of ɛ4 in the association between ongoing episodic memory decline and olfactory deficits in the general population, but such information is relevant in determining the relevance of olfaction as a marker of DAT risk. The present study was based on a large, population-based sample (n=1087, aged 45-90 years, of which 324 were ɛ4-carriers). Episodic memory change rates were established using data collected every 5 years for a 10-20 year interval leading up to an olfactory assessment using the Scandinavian Odor Identification Test at the last wave of data collection. Participants were classified according to whether or not their episodic memory ability declined more rapidly than the age-typical norm (by > 1SD). Our main result is that only in ɛ4-carriers was episodic memory decline associated with odor identification impairment. In individuals without ɛ4, odor identification was unrelated to episodic memory decline status. Follow-up analyses indicated that this moderation by ɛ4 was due to the olfactory nature of the identification test, and that the effect was not caused by 63 individuals with dementia. Our results suggest that the ɛ4 determines the functional association between ongoing episodic memory decline and olfaction. These findings are consistent with the notion that ɛ4-carriers with DAT, compared to non-carriers, display a cortical atrophy pattern that is more focused on mediotemporal lobe regions supporting olfactory and episodic memory functions. Olfactory and memory assessments might provide complementary information on mediotemporal atrophy prior to clinical dementia onset, but the ɛ4 should be considered when using olfactory assessment as an early-stage indicator.

  • 114.
    Olsson, Jan
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Kok, Eloise
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Lövheim, Hugo
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Elgh, Fredrik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Herpes virus seroepidemiology in the adult Swedish population2017Ingår i: Immunity & Ageing, ISSN 1742-4933, E-ISSN 1742-4933, Vol. 14, artikel-id 10Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Herpes viruses establish a life-long latency and can cause symptoms during both first-time infection and later reactivation. The aim of the present study was to describe the seroepidemiology of Herpes simplex type 1 (HSV1), Herpes simplex type 2 (HSV2), Cytomegalovirus (CMV), Varicella Zoster virus (VZV) and Human herpes virus type 6 (HHV6) in an adult Swedish population (35-95 years of age). Methods: Presence of antibodies against the respective viruses in serum from individuals in the Betula study was determined with an enzyme-linked immunosorbent assay (ELISA). Singular samples from 535 persons (53.9% women, mean age at inclusion 62.7 +/- 14.4 years) collected 2003-2005 were analyzed for the five HHVs mentioned above. In addition, samples including follow-up samples collected 1988-2010 from 3,444 persons were analyzed for HSV. Results: Prevalence of HSV1 was 79.4%, HSV2 12.9%, CMV 83.2%, VZV 97.9%, and HHV6 97.5%. Herpes virus infections were more common among women (p = 0.010) and a lower age-adjusted HSV seroprevalence was found in later birth cohorts (p < 0.001). The yearly incidence of HSV infection was estimated at 14.0/1000. Conclusion: Women are more often seropositive for HHV, especially HSV2. Age-adjusted seroprevalence for HSV was lower in later birth cohorts indicating a decreasing childhood and adolescent risk of infection.

  • 115.
    Oudin, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa. Department of Laboratory Medicine, Lund University, Lund, Sweden..
    Andersson, John
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Sundström, Anna
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Oudin Åström, Daniel
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Forsberg, Bertil
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Traffic-Related Air Pollution as a Risk Factor for Dementia: No Clear Modifying Effects of APOEɛ4 in the Betula Cohort2019Ingår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 71, nr 3, s. 733-740Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    It is widely known that the apolipoprotein E (APOE) ɛ4 allele imposes a higher risk for Alzheimer’s disease (AD). Recent evidence suggests that exposure to air pollution is also a risk factor for AD, and results from a few studies indicate that the effect of air pollution on cognitive function and dementia is stronger in APOE ɛ4 carriers than in non-carriers. Air pollution and interaction with APOE ɛ4 on AD risk thus merits further attention. We studied dementia incidence over a 15-year period from the longitudinal Betula study in Northern Sweden. As a marker for long-term exposure to traffic-related air pollution, we used modelled annual mean nitrogen oxide levels at the residential address of the participants at start of follow-up. Nitrogen oxide correlate well with fine particulate air pollution levels in the study area. We had full data on air pollution, incidence of AD and vascular dementia (VaD), APOE ɛ4 carrier status, and relevant confounding factors for 1,567 participants. As expected, air pollution was rather clearly associated with dementia incidence. However, there was no evidence for a modifying effect by APOE ɛ4 on the association (p-value for interaction > 0.30 for both total dementia (AD+VaD) and AD). The results from this study do not imply that adverse effects of air pollution on dementia incidence is limited to, or stronger in, APOE ɛ4 carriers than in the total population.

  • 116.
    Oudin, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Forsberg, Bertil
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Lind, Nina
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Modig, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nordin, Steven
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI). Aging research centre, Karolinska Institutet.
    Traffic-Related Air Pollution and Dementia Incidence in Northern Sweden: A Longitudinal Study2016Ingår i: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 124, nr 3, s. 306-312Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Exposure to ambient air pollution is suspected to cause cognitive effects, but a prospective cohort is needed to study exposure to air pollution at the home address and the incidence of dementia.

    OBJECTIVES: We aimed to assess the association between long-term exposure to traffic-related air pollution and dementia incidence in a major city in northern Sweden.

    METHODS: Data on dementia incidence over a 15-year period were obtained from the longitudinal Betula study. Traffic air pollution exposure was assessed with a Land Use Regression Model with a spatial resolution of 50 m x 50 m. Annual mean nitrogen oxide levels at the residential address of the participants at baseline (the start of follow-up) was used as a marker for long-term exposure to air pollution.

    RESULTS: Out of 1806 participants at baseline, 191 were diagnosed with Alzheimer's disease during follow-up, and 111 were diagnosed with vascular dementia. Participants in the highest exposure group were more likely to be diagnosed with dementia (Alzheimer's disease or vascular dementia), with a Hazard Ratio (HR) of 1.43 (95% Confidence Interval (CI): 0.998, 2.05 for the highest versus lowest quartile). The estimates were similar for Alzheimer's disease (HR 1.38) and vascular dementia (HR 1.47). The HR for dementia associated for the third quartile versus the lowest quartile was 1.48 (95% CI: 1.03, 2.11). A sub-analysis that excluded a younger sample that had been re-tested after only 5 years of follow-up suggested stronger associations with exposure than in the full cohort (HR = 1.71; 95% CI: 1.08, 2.73 for the highest versus lowest quartile).

    CONCLUSIONS: If the associations we observed are causal, then air pollution from traffic might be an important risk factor for vascular dementia and Alzheimer's disease.

  • 117.
    Oudin, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Segersson, David
    Swedish Meteorological and Hydrological Institute, Norrköping, Sweden.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Forsberg, Bertil
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Association between air pollution from residential wood burning and dementia incidence in a longitudinal study in Northern Sweden2018Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 13, nr 6, artikel-id e0198283Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVES: There is highly suggestive evidence for an effect of air pollution exposure on dementia-related outcomes, but evidence is not yet present to clearly pinpoint which pollutants are the probable causal agents. The aims of this study was to assess the longitudinal association between exposures of fine ambient particulate matter (PM2.5) from residential wood burning, and vehicle exhaust, with dementia.

    METHOD: We used data from the Betula study, a longitudinal study of dementia in Umeå, Northern Sweden. The study size was 1 806 and the participants were followed from study entry (1993-1995) to 2010. Modelled levels of source-specific fine particulate matter at the residential address were combined with information on wood stoves or wood boilers, and with validated data on dementia diagnosis and individual-level characteristics from the Betula study. Cox proportional hazards models were used to estimate Hazard Ratios (HRs) and their 95% CIs for dementia incidence (vascular dementia and Alzheimer's disease), adjusted for individual-level characteristics.

    RESULTS: The emission of PM2.5 from local residential wood burning was associated with dementia incidence with a hazard ratio of 1.55 for a 1 μg/m3 increase in PM2.5 (95% Confidence Interval (CI): 1.00-2.41, p-value 0.05). Study participants with an address in an area with the highest quartile of PM2.5 from residential wood burning and who also had a wood-burning stove were more likely to develop dementia than those in the lower three quartiles without a wood-burning stove with hazard ratios of 1.74 (CI: 1.10-2.75, p-value 0.018). Particulate matter from traffic exhaust seemed to be associated with dementia incidence with hazard ratios of 1.66, (CI: 1.16-2.39), p-value 0.006, and 1.41 (CI: 0.97-2.23), p-value 0.07, in the third and fourth quartiles, respectively.

    CONCLUSIONS: If the associations we observed are causal, then air pollution from residential wood burning, and air pollution from traffic, might be independent important risk factors for dementia.

  • 118. Partonen, Timo
    et al.
    Treutlein, Jens
    Alpman, Asude
    Frank, Josef
    Johansson, Carolina
    Depner, Martin
    Aron, Liviu
    Rietschel, Marcella
    Wellek, Stefan
    Soronen, Pia
    Paunio, Tiina
    Koch, Andreas
    Chen, Ping
    Lathrop, Mark
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Persson, Maj-Liz
    Kasper, Siegfried
    Schalling, Martin
    Peltonen, Leena
    Schumann, Gunter
    Three circadian clock genes Per2, Arnt1, and Npas2 contribute to winter depression2007Ingår i: Annals of Medicine, ISSN 0785-3890, E-ISSN 1365-2060, Vol. 39, nr 3, s. 229-238Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Multiple lines of evidence suggest that the circadian clock contributes to the pathogenesis of winter depression or seasonal affective disorder (SAD). We hypothesized that sequence variations in three genes, including Per2, Arntl, and Npas2, which form a functional unit at the core of the circadian clock, predispose to winter depression.

    Methods. In silico analysis of the biological effects of allelic differences suggested the target single-nucleotide polymorphisms (SNPs) to be analyzed in a sample of 189 patients and 189 matched controls. The most relevant SNP in each gene was identified for the interaction analysis and included in the multivariate assessment of the combined effects of all three SNPs on the disease risk.

    Results. SAD was associated with variations in each of the three genes in gene-wise logistic regression analysis. In combination analysis of variations of Per2, Arntl, and Npas2, we found additive effects and identified a genetic risk profile for the disorder. Carriers of the risk genotype combination had the odds ratio of 4.43 of developing SAD as compared with the remaining genotypes, and of 10.67 as compared with the most protective genotype combination.

    Conclusion. Variations in the three circadian clock genes Per2, Arntl, and Npas2 are associated with the disease, supporting the hypothesis that the circadian clock mechanisms contribute to winter depression.

  • 119. Persson, J.
    et al.
    Lind, J.
    Larsson, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Radiofysik.
    Ingvar, M.
    Sleegers, K.
    Van Broeckhoven, C.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, L.-G.
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Diagnostisk radiologi. Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB).
    Altered deactivation in individuals with genetic risk for Alzheimer's disease2008Ingår i: Neuropsychologia, ISSN 0028-3932, E-ISSN 1873-3514, Vol. 46, nr 6, s. 1679-1687Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Regions that show task-induced deactivations may be part of a default-mode network related to processes that are more engaged during passive than active task conditions. Alteration of task-induced deactivations with age and dementia is indicated by atypical engagement of default-mode network regions. Genetic studies show a relation between the apolipoprotein E4 (APOE4) allele and the common form of Alzheimer's disease (AD), and altered functional brain activation has been observed in non-demented APOE4 carriers compared to non-carriers. Here we investigate the hypothesis of altered default-mode network brain responses in individuals with genetic risk for AD. Functional MRI was used to assess task-induced deactivation in 60 subjects of which 30 carried at least one copy of the APOE4 allele, and 30 non-carriers. Subjects were scanned while performing a semantic categorization task shown to promote episodic memory encoding. The results show patterns of deactivation consistent with the default-mode network. We also found reduced deactivation in non-demented APOE4 carriers compared to non-carriers, suggesting alterations in the default-mode network in the absence of dementia. These results implicate possibilities for investigating altered properties of task-induced deactivations in individuals with genetic risk for AD, and may prove useful for pre-clinical identification of individuals susceptible to memory problems and AD.

  • 120.
    Persson, Jonas
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Lind, Johanna
    Larsson, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Radiofysik.
    Ingvar, Martin
    Cruts, Marc
    Van Broeckhoven, Christine
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    Nyberg, Lars
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Altered brain white matter integrity in healthy carriers of the APOE epsilon4 allele: A risk for AD?2006Ingår i: Neurology, Vol. 66, s. 1029-1033Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Previous research has shown that polymorphisms of apolipoprotein E (APOE) represent genetic risk factors for dementia and for cognitive impairment in the elderly. The neural mechanisms by which these genetic variations influence behavioral performance or clinical severity are not well understood.

    METHODS: The authors used diffusion tensor imaging to investigate ultrastructural properties in brain white matter to detect pathologic processes that modify tissue integrity. Sixty participants were included in the study of which 30 were homozygous for the APOE epsilon3 allele, 10 were homozygous for the APOE epsilon4 allele, and 20 had the APOE epsilon34 allele combination. All individuals were non-demented, and the groups were matched on demographic variables and cognitive performance.

    RESULTS: The results showed a decline in fractional anisotropy, a marker for white matter integrity, in the posterior corpus callosum of epsilon4 carriers compared to non-carriers. Additional sites of altered white matter integrity included the medial temporal lobe.

    CONCLUSIONS: Although the mechanism underlying vulnerability of white matter tracts in APOE epsilon4 carriers is still unknown, these findings suggest that increased genetic risk for developing Alzheimer disease is associated with changes in microscopic white matter integrity well before the onset of dementia.

  • 121. Pickard, Benjamin Simon
    et al.
    Van Den Bossche, Maarten J. A.
    Malloy, Mary P.
    Johnstone, Mandy
    Lenaerts, An-Sofie
    Nordin, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Goossens, Dirk
    St Clair, David
    Muir, Walter J.
    Nilsson, Lars-Goran
    Sabbe, Bernard
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Blackwood, Douglas H. R.
    Del-Favero, Jurgen
    Multiplex amplicon quantification screening the ABCA13 gene for copy number variation in schizophrenia and bipolar disorder2012Ingår i: Psychiatric Genetics, ISSN 0955-8829, E-ISSN 1473-5873, Vol. 22, nr 5, s. 269-270Artikel i tidskrift (Refereegranskat)
  • 122. Rademakers, R
    et al.
    Sleegers, K
    Theuns, J
    Van den Broeck, M
    Kacem, S B
    Nilsson, L G
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    van Duijn, C M
    Van Broeckhoven, C
    Cruts, M
    Association of cyclin-dependent kinase 5 and neuronal activators p35 and p39 complex in early-onset Alzheimer's disease2005Ingår i: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 26, nr 8, s. 1145-1151Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Malfunctioning of cyclin-dependent kinase 5 (CDK5) through aberrant proteolytic cleavage of its neuronal activators p35 and p39 is involved in neurodegeneration in Alzheimer's disease (AD) and other neurodegenerative brain diseases. By extensive genetic analysis of the genes encoding CDK5 (CDK5), p35 (CDK5RI) and p39 (CDK5R2), we excluded causal mutations in 70 familial early-onset AD patients. We performed an association study with five informative SNPs in CDK5 in two independent samples of early-onset AD patients and matched control individuals from The Netherlands and northern Sweden. Association was observed with g.149800G > C in intron 5 of CDK5, and a two times increased risk was observed in both patient samples for carriers of the C-allele. Our data are indicative for a role of the CDK5 molecular complex in the genetic etiology of early-onset AD, and suggest that a yet unknown functional variant in CDK5 or in a nearby gene might lead to increased susceptibility for early-onset AD.

  • 123. Ripke, Stephan
    et al.
    Neale, Benjamin M.
    Corvin, Aiden
    Walters, James T. R.
    Farh, Kai-How
    Holmans, Peter A.
    Lee, Phil
    Bulik-Sullivan, Brendan
    Collier, David A.
    Huang, Hailiang
    Pers, Tune H.
    Agartz, Ingrid
    Agerbo, Esben
    Albus, Margot
    Alexander, Madeline
    Amin, Farooq
    Bacanu, Silviu A.
    Begemann, Martin
    Belliveau, Richard A., Jr.
    Bene, Judit
    Bergen, Sarah E.
    Bevilacqua, Elizabeth
    Bigdeli, Tim B.
    Black, Donald W.
    Bruggeman, Richard
    Buccola, Nancy G.
    Buckner, Randy L.
    Byerley, William
    Cahn, Wiepke
    Cai, Guiqing
    Campion, Dominique
    Cantor, Rita M.
    Carr, Vaughan J.
    Carrera, Noa
    Catts, Stanley V.
    Chambert, Kimberly D.
    Chan, Raymond C. K.
    Chen, Ronald Y. L.
    Chen, Eric Y. H.
    Cheng, Wei
    Cheung, Eric F. C.
    Chong, Siow Ann
    Cloninger, C. Robert
    Cohen, David
    Cohen, Nadine
    Cormican, Paul
    Craddock, Nick
    Crowley, James J.
    Curtis, David
    Davidson, Michael
    Davis, Kenneth L.
    Degenhardt, Franziska
    Del Favero, Jurgen
    Demontis, Ditte
    Dikeos, Dimitris
    Dinan, Timothy
    Djurovic, Srdjan
    Donohoe, Gary
    Drapeau, Elodie
    Duan, Jubao
    Dudbridge, Frank
    Durmishi, Naser
    Eichhammer, Peter
    Eriksson, Johan
    Escott-Price, Valentina
    Essioux, Laurent
    Fanous, Ayman H.
    Farrell, Martilias S.
    Frank, Josef
    Franke, Lude
    Freedman, Robert
    Freimer, Nelson B.
    Friedl, Marion
    Friedman, Joseph I.
    Fromer, Menachem
    Genovese, Giulio
    Georgieva, Lyudmila
    Giegling, Ina
    Giusti-Rodriguez, Paola
    Godard, Stephanie
    Goldstein, Jacqueline I.
    Golimbet, Vera
    Gopal, Srihari
    Gratten, Jacob
    de Haan, Lieuwe
    Hammer, Christian
    Hamshere, Marian L.
    Hansen, Mark
    Hansen, Thomas
    Haroutunian, Vahram
    Hartmann, Annette M.
    Henskens, Frans A.
    Herms, Stefan
    Hirschhorn, Joel N.
    Hoffmann, Per
    Hofman, Andrea
    Hollegaard, Mads V.
    Hougaard, David M.
    Ikeda, Masashi
    Joa, Inge
    Julia, Antonio
    Kahn, Rene S.
    Kalaydjieva, Luba
    Karachanak-Yankova, Sena
    Karjalainen, Juha
    Kavanagh, David
    Keller, Matthew C.
    Kennedy, James L.
    Khrunin, Andrey
    Kim, Yunjung
    Klovins, Janis
    Knowles, James A.
    Konte, Bettina
    Kucinskas, Vaidutis
    Kucinskiene, Zita Ausrele
    Kuzelova-Ptackova, Hana
    Kahler, Anna K.
    Laurent, Claudine
    Keong, Jimmy Lee Chee
    Lee, S. Hong
    Legge, Sophie E.
    Lerer, Bernard
    Li, Miaoxin
    Li, Tao
    Liang, Kung-Yee
    Lieberman, Jeffrey
    Limborska, Svetlana
    Loughland, Carmel M.
    Lubinski, Jan
    Lonnqvist, Jouko
    Macek, Milan, Jr.
    Magnusson, Patrik K. E.
    Maher, Brion S.
    Maier, Wolfgang
    Mallet, Jacques
    Marsal, Sara
    Mattheisen, Manuel
    Mattingsdal, Morten
    McCarley, Robert W.
    McDonald, Colm
    McIntosh, Andrew M.
    Meier, Sandra
    Meijer, Carin J.
    Melegh, Bela
    Melle, Ingrid
    Mesholam-Gately, Raquelle I.
    Metspalu, Andres
    Michie, Patricia T.
    Milani, Lili
    Milanova, Vihra
    Mokrab, Younes
    Morris, Derek W.
    Mors, Ole
    Murphy, Kieran C.
    Murray, Robin M.
    Myin-Germeys, Inez
    Mueller-Myhsok, Bertram
    Nelis, Mari
    Nenadic, Igor
    Nertney, Deborah A.
    Nestadt, Gerald
    Nicodemus, Kristin K.
    Nikitina-Zake, Liene
    Nisenbaum, Laura
    Nordin, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    O'Callaghan, Eadbhard
    O'Dushlaine, Colm
    O'Neill, F. Anthony
    Oh, Sang-Yun
    Olincy, Ann
    Olsen, Line
    Van Os, Jim
    Pantelis, Christos
    Papadimitriou, George N.
    Papiol, Sergi
    Parkhomenko, Elena
    Pato, Michele T.
    Paunio, Tiina
    Pejovic-Milovancevic, Milica
    Perkins, Diana O.
    Pietilainen, Olli
    Pimm, Jonathan
    Pocklington, Andrew J.
    Powell, John
    Price, Alkes
    Pulver, Ann E.
    Purcell, Shaun M.
    Quested, Digby
    Rasmussen, Henrik B.
    Reichenberg, Abraham
    Reimers, Mark A.
    Richards, Alexander L.
    Roffman, Joshua L.
    Roussos, Panos
    Ruderfer, Douglas M.
    Salomaa, Veikko
    Sanders, Alan R.
    Schall, Ulrich
    Schubert, Christian R.
    Schulze, Thomas G.
    Schwab, Sibylle G.
    Scolnick, Edward M.
    Scott, Rodney J.
    Seidman, Larry J.
    Shi, Jianxin
    Sigurdsson, Engilbert
    Silagadze, Teimuraz
    Silverman, Jeremy M.
    Sim, Kang
    Slominsky, Petr
    Smoller, Jordan W.
    So, Hon-Cheong
    Spencer, Chris C. A.
    Stahl, Eli A.
    Stefansson, Hreinn
    Steinberg, Stacy
    Stogmann, Elisabeth
    Straub, Richard E.
    Strengman, Eric
    Strohmaier, Jana
    Stroup, T. Scott
    Subramaniam, Mythily
    Suvisaari, Jaana
    Svrakic, Dragan M.
    Szatkiewicz, Jin P.
    Soderman, Erik
    Thirumalai, Srinivas
    Toncheva, Draga
    Tosato, Sarah
    Veijola, Juha
    Waddington, John
    Walsh, Dermot
    Wang, Dai
    Wang, Qiang
    Webb, Bradley T.
    Weiser, Mark
    Wildenauer, Dieter B.
    Williams, Nigel M.
    Williams, Stephanie
    Witt, Stephanie H.
    Wolen, Aaron R.
    Wong, Emily H. M.
    Wormley, Brandon K.
    Xi, Hualin Simon
    Zai, Clement C.
    Zheng, Xuebin
    Zimprich, Fritz
    Wray, Naomi R.
    Stefansson, Kari
    Visscher, Peter M.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Andreassen, Ole A.
    Blackwood, Douglas H. R.
    Bramon, Elvira
    Buxbaum, Joseph D.
    Borglum, Anders D.
    Cichon, Sven
    Darvasi, Ariel
    Domenici, Enrico
    Ehrenreich, Hannelore
    Esko, Tonu
    Gejman, Pablo V.
    Gill, Michael
    Gurling, Hugh
    Hultman, Christina M.
    Iwata, Nakao
    Jablensky, Assen V.
    Jonsson, Erik G.
    Kendler, Kenneth S.
    Kirov, George
    Knight, Jo
    Lencz, Todd
    Levinson, Douglas F.
    Li, Qingqin S.
    Liu, Jianjun
    Malhotra, Anil K.
    McCarroll, Steven A.
    McQuillin, Andrew
    Moran, Jennifer L.
    Mortensen, Preben B.
    Mowry, Bryan J.
    Noethen, Markus M.
    Ophoff, Roel A.
    Owen, Michael J.
    Palotie, Aarno
    Pato, Carlos N.
    Petryshen, Tracey L.
    Posthuma, Danielle
    Rietschel, Marcella
    Riley, Brien P.
    Rujescu, Dan
    Sham, Pak C.
    Sklar, Pamela
    St Clair, David
    Weinberger, Daniel R.
    Wendland, Jens R.
    Werge, Thomas
    Daly, Mark J.
    Sullivan, Patrick F.
    O'Donovan, Michael C.
    Biological insights from 108 schizophrenia-associated genetic loci2014Ingår i: Nature, ISSN 0028-0836, E-ISSN 1476-4687, Vol. 511, nr 7510, s. 421-427Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.

  • 124.
    Rönnlund, Michael
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Sundström, Anna
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Umeå universitet, Samhällsvetenskapliga fakulteten, Enheten för demografi och åldrandeforskning (CEDAR).
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI). Aging Research Center, Karolinska Institutet, Stockholm, Sweden.
    Self-reported memory failures: associations with future dementia in a population-based study with long-term follow-up2015Ingår i: Journal of The American Geriatrics Society, ISSN 0002-8614, E-ISSN 1532-5415, Vol. 63, nr 9, s. 1766-1773Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVES: To examine the association between self-reported memory failures and incident dementia in individuals aged 60 and older.

    DESIGN: Longitudinal, community based.

    SETTING: Betula Prospective Cohort Study, a population-based study in Umea, Sweden.

    PARTICIPANTS: Individuals with a mean age of 71.5 +/- 8.8 (range 60-90) (N = 1,547).

    MEASUREMENTS: Participants rated the frequency of everyday memory failures using the 16-item Prospective and Retrospective Memory Questionnaire (PRMQ) and underwent objective memory testing at baseline. Participant self-reports of complaints of poor memory by family and friends were evaluated. Dementia status was followed-up for 10 to 12 years.

    RESULTS: Over the study period, 225 participants developed dementia (132 with Alzheimer's disease (AD)). In Cox proportional hazard regression models adjusted for demographic factors, PRMQ z-scores predicted incident dementia (hazard ratio (HR) = 1.21 for all-cause dementia; HR = 1.25 for AD, Ps < .01). The significant associations remained when depressive symptoms and objective memory performance were adjusted for, when low performers on objective memory (= 1 standard deviations below the age group mean) were excluded, and in analyses with delayed entry (survival time = 5 years). Similar patterns were observed for the prospective and retrospective subscales, although including how often participants self-reported that others complained about their poor memory eliminated the association between PRMQ scores and dementia and itself emerged as a significant predictor.

    CONCLUSION: Self-reported memory failure predicted future dementia or AD independent of objective memory performance. Subjective reports of complaints by family and friends appear to be an even more-important indicator of preclinical impairments, and physicians should not ignore them, even in the absence of objective memory deficits.

  • 125.
    Rönnlund, Michael
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Sundström, Anna
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Umeå universitet, Samhällsvetenskapliga fakulteten, Enheten för demografi och åldrandeforskning (CEDAR).
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI). Aging Research Center, Karolinska Institutet, Stockholm, Sweden.
    Subjective memory impairment in older adults predicts future dementia independent of baseline memory performance: Evidence from the Betula prospective cohort study2015Ingår i: Alzheimer's & Dementia, ISSN 1552-5260, E-ISSN 1552-5279, Vol. 11, nr 11, s. 1385-1392Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    INTRODUCTION: The objective was to examine whether subjective memory impairment (SMI) predicts all-cause dementia or Alzheimer's disease (AD) in a population-based study with long-term follow-up (median = 10 years).

    METHODS: A total of 2043 initially dementia-free participants (≥ 60 years) made three memory ratings ("compared with others", "compared with five years ago", and "complaints from family/friends") at baseline. During follow-up, 372 participants developed dementia (208 with AD).

    RESULTS: Cox regression revealed that subjective memory impairment ratings predicted all-cause dementia in models adjusting for age and sex (hazard ratio or HR from 2.04 to 3.94), with even higher values for AD (HR from 2.29 to 5.74). The result persisted in models including other covariates, including baseline episodic memory performance, and in analyses restricted to participants with long time to dementia diagnosis (≥ 5 years).

    DISCUSSION: The findings underscore the usefulness of subjective memory assessment in combination with other factors in identifying individuals at risk for developing dementia.

  • 126.
    Rönnlund, Michael
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Åström, Elisabeth
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Carelli, Maria Grazia
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Perceived stress in adults aged 65 to 90: Relations to facets of time perspective and COMT Val158Met polymorphism2018Ingår i: Frontiers in Psychology, ISSN 1664-1078, E-ISSN 1664-1078, Vol. 9, artikel-id 378Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    This study examined the relation between perceived stress and time perspective (views of past, present, future) in a population-based sample of older adults (65-90 years, N = 340). The Perceived Questionnaire (PSQ index) was used to measure stress and the Swedish version of the Zimbardo Time Perspective Inventory (S-ZTPI) was used to operationalize time perspective. Unlike the original inventory, S-ZTPI separates positive and negative aspects of a future time perspective and we hypothesized that the Future Negative (FN) scale would be important to account for variations in stress. Additionally, associations with Catechol-O-methyltransferase (COMT) Val(158)Met polymorphism were examined, motivated by prior associations of this single nucleotide polymorphism (SNP) with stress (or "anxiety") related personality traits. In line with the hypotheses, FN was the strongest predictor of PSQ index scores in multiple regression analyses. In a related vein, the dichotomization of the unitary Future scale increased the association between PSQ scores and a measure of deviations from a balanced time perspective, i.e., the difference between a proposed optimal and observed ZTPI profile. Finally, higher levels of stress as well as higher scores on FN were observed in COMT Val/Val carriers, at least among men. This suggests a shared dopaminergic genetic influence on these variables. Collectively, the results demonstrate that perceived stress is closely linked to time perspective and highlight the need to take negative aspects of a future temporal orientation into account to understand this relation.

  • 127.
    Sandman, Per-Olof
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för omvårdnad.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Nygren, Charlotte
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för kostvetenskap.
    Nyström, Lennarth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa.
    Winblad, Bengt
    Umeå universitet.
    Treatment of constipation with high-bran bread in long-term care of severly demented elderly patients1983Ingår i: Journal of The American Geriatrics Society, ISSN 0002-8614, E-ISSN 1532-5415, Vol. 31, nr 5, s. 289-293Artikel i tidskrift (Refereegranskat)
  • 128.
    Sandman, Per-Olof
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för omvårdnad.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Norberg, Astrid
    Umeå universitet, Medicinska fakulteten, Institutionen för omvårdnad.
    Nyström, Lennarth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa.
    Winblad, Bengt
    Umeå universitet.
    Long-term care of the elderly: A descriptive study of 3600 institutionalized patients in the county of Västerbotten, Sweden1988Ingår i: Comprehensive gerontology. Section A, Clinical and laboratory sciences, ISSN 0902-0071, Vol. 2, nr 3, s. 120-32Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Probands (n = 3607) living in long-term care institutions in the county of Västerbotten were assessed to estimate whether the prevalence of dementia in different types of institutions had changed since a similar survey was made 7 years before. The probands' motoric functions, vision, hearing, speech, prevalence of behavioral disturbances and psychiatric symptoms, work load and use of psychoactive drugs were also investigated with special emphasis on the differences between the demented and the non-demented. About 40% were demented. This proportion of demented patients had increased in somatic long-stay clinics, nursing homes and homes for the aged since 1975. Further, the mean age of the probands and their length of stay had increased in these institutions. Demented probands were more impaired with regard to motor functions, speech, vision, hearing, ADL-functions, behavioral and psychiatric symptoms, and they also imposed a higher work load on the staff than the non-demented. Demented probands were also prescribed psychoactive drugs, i.e. neuroleptics but not minor tranquilizers or antidepressants, more often than the non-demented in accordance with the increased prevalence of behavioral disturbances and psychiatric symptoms.

  • 129.
    Sandman, Per-Olof
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för omvårdnad.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nygren, Charlotte
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för kostvetenskap.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Winblad, Bengt
    Umeå universitet.
    Nutritional status and dietary intake in institutionalised patients with Alzheimer's disease and multifarct dementia1987Ingår i: Journal of The American Geriatrics Society, ISSN 0002-8614, E-ISSN 1532-5415, Vol. 35, s. 31-38Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Nutritional status, dietary intake, weight change, and mortality were studied in a sample of severely demented, institutionalized patients. Dietary intake was registered during five days in two periods, five weeks apart. A weighing method was used. Nutritional status was assessed by anthropometric measurements (weight for height index, triceps skinfold thickness, arm muscle circumference) and determination of circulating proteins (albumin, transferrin, and prealbumin). Energy and/or protein malnutrition was found in 50% of the patients. The mean dietary intake was sufficient according to energy (2059 kcal/day), proteins, vitamins, and minerals. A comparison of patients with or without malnutrition showed no differences in dietary intake, diagnoses, age, length of hospital stay, or duration of illness. However, malnourished patients had had four times as many infectious periods treated by antibiotics as patients with no malnutrition. Thirty-nine of 44 patients lost weight during their hospital stay. There was no correlation between loss of weight, length of hospital stay, or duration of illness.

  • 130.
    Sandman, Per-Olof
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för omvårdnad.
    Norberg, Astrid
    Umeå universitet, Medicinska fakulteten, Institutionen för omvårdnad.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Verbal communication and behaviour during meals in five institutionalized patients with Alzheimer-type dementia1988Ingår i: Journal of Advanced Nursing, ISSN 0309-2402, E-ISSN 1365-2648, Vol. 13, nr 5, s. 571-578Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Five institutionalized patients with Alzheimer-type dementia were observed (video-recorded) during meals. The aim was to assess their meal behaviour and social interaction. The results showed that when the patients ate without the participation of staff, the two least demented patients became 'caregivers' in the group and helped the three most demented patients to eat. When two mental nurses joined the group, the patients dropped their roles as helpers. The conversation in the group could be characterized as incomplete, with short sentences and a lot of breaks. Sixty-three per cent of all comprehensible utterances concerned food and eating and almost all conversation concerned the present.

  • 131.
    Sandman, Per-Olof
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för omvårdnad. Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Norberg, Astrid
    Umeå universitet, Medicinska fakulteten, Institutionen för omvårdnad.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Axelsson, Karin
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Hedly, V
    Nursing College. University of Stockholm, Stockholm, Sweden.
    Morning care of patients with Alzheimer-type dementia: A theoretical model based on direct observations1986Ingår i: Journal of Advanced Nursing, ISSN 0309-2402, E-ISSN 1365-2648, Vol. 11, nr 4, s. 369-378Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Five hospitalized patients in different stages of Alzheimer-type dementia were monitored by unstructured, direct observations during morning care. Orem's model of nursing as a compensation for the patient's lack of self-care capabilities was used as a frame of reference for an analysis of the behaviours of patients and nurses during morning care. A 12-step classification system was developed to be used as a guide to understand and determine abilities essential for performance of morning care for demented patients. The quantitative assessment showed that none of the patients was able to manage morning care independently, but there was a wide variation in their highest level of performance.

  • 132. Schlaepfer, T E
    et al.
    Frick, C
    Zobel, A
    Maier, W
    Heuser, I
    Bajbouj, M
    O'Keane, V
    Corcora, C
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Trimble, M
    Rau, H
    Hoff, H J
    Padberg, F
    Müller-Siecheneder, F
    Audenaert, K
    Van den Abbeele, D
    Matthews, K
    Christmas, D
    Stanga, Z
    Hasdemir, M
    Vagus nerve stimulation for depression: Efficacy and safety in a European study.2008Ingår i: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 38, nr 5, s. 651-661Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Vagus nerve stimulation (VNS) therapy is associated with a decrease in seizure frequency in partial-onset seizure patients. Initial trials suggest that it may be an effective treatment, with few side-effects, for intractable depression. Method: An open, uncontrolled European multi-centre study (D03) of VNS therapy was conducted, in addition to stable pharmacotherapy, in 74 patients with treatment-resistant depression (TRD). Treatment remained unchanged for the first 3 months; in the subsequent 9 months, medications and VNS dosing parameters were altered as indicated clinically. Results: The baseline 28-item Hamilton Depression Rating Scale (HAMD-28) score averaged 34. After 3 months of VNS, response rates (≥50% reduction in baseline scores) reached 37% and remission rates (HAMD-28 score <10) 17%. Response rates increased to 53% after 1 year of VNS, and remission rates reached 33%. Response was defined as sustained if no relapse occurred during the first year of VNS after response onset; 44% of patients met these criteria. Median time to response was 9 months. Most frequent side-effects were voice alteration (63% at 3 months of stimulation) and coughing (23%). Conclusions: VNS therapy was effective in reducing severity of depression; efficacy increased over time. Efficacy ratings were in the same range as those previously reported from a USA study using a similar protocol; at 12 months, reduction of symptom severity was significantly higher in the European sample. This might be explained by a small but significant difference in the baseline HAMD-28 score and the lower number of treatments in the current episode in the European study.

  • 133. Sköld, Mia
    et al.
    Källstrand, Johan
    Nehlstedt, Sara
    Nordin, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nielzén, Sören
    Holmberg, Jens
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Thalamocortical abnormalities in auditory brainstem response patterns distinguish DSM-IV bipolar disorder type I from schizophrenia2014Ingår i: Journal of Affective Disorders, ISSN 0165-0327, E-ISSN 1573-2517, Vol. 169, s. 105-11Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Bipolar disorder type I (BP-I) belongs to a spectrum of affective disorders that are expressed in many different ways and therefore can be difficult to distinguish from other conditions, especially unipolar depression, schizoaffective disorder, schizophrenia (SZ), but also anxiety and personality disorders. Since early diagnosis and treatment have shown to improve the long-term prognosis, complementary specific biomarkers are of great value. The auditory brainstem response (ABR) has previously been applied successfully to identify specific abnormal ABR patterns in SZ and Asperger syndrome.

    METHODS: The current study investigated the early auditory processing of complex sound stimuli e.g. forward masking, in BP-I compared to SZ patients. The ABR curves of BP-I patients (n=23) and SZ patients (n=20) were analyzed in terms of peak amplitudes and correlation with an ABR norm curve based on a non-psychiatric control group (n=20).

    RESULTS: BP-I patients had significantly higher wave III (p=0.0062) and wave VII (p=0.0472) amplitudes compared with SZ patients. Furthermore, BP-I patients, and to a lesser extent SZ patients, showed low correlation with the norm ABR curve in the part of the curve comprising waves VI-VII.

    LIMITATIONS: Sample size was relatively small and study groups were not matched for age and gender.

    CONCLUSIONS: BP-I patients showed specific aberrances, specifically in the latter part of the ABR curve, implicating abnormalities in thalamocortical circuitry. The abnormal ABR wave patterns significantly separated BP-I patients from SZ patients suggesting that ABR might serve as a biomarker for BP-I.

  • 134. Smedh, K
    et al.
    Spigset, O
    Allard, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Mjörndal, T
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Platelet [3H]paroxetine and [3H]lysergic acid diethylamide binding in seasonal affective disorder and the effect of bright light therapy.1999Ingår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 45, nr 4, s. 464-70Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Seasonal affective disorder (SAD) has been regarded as a melatonin disorder, but the pathophysiological mechanisms of SAD are to a large extent unclarified. Serotonergic mechanisms have also been studied, but they have shown inconsistent results. METHODS: We have compared [3H]paroxetine and [3H]lysergic acid diethylamide (LSD) binding in platelets from 23 SAD patients and 23 controls. Then SAD patients had 4 weeks of light therapy. On the last treatment day new blood samples were drawn. Symptoms before and after light treatment were measured by SIGH-SAD. RESULTS: Bmax for paroxetine binding before light treatment was higher in SAD patients compared to controls and also higher in responders than in nonresponders. Bmax decreased significantly during light treatment. We also found a negative correlation between the two Bmax values before but not after light treatment. There was a negative correlation between Bmax for paroxetine binding before treatment and clinical status after treatment. Patients with reduced Bmax for LSD binding after treatment had a better clinical treatment response. CONCLUSIONS: The present study indicates that serotonin receptor parameters might be suitable in the prediction of clinical response to light treatment.

  • 135. Stahl, Eli A.
    et al.
    Breen, Gerome
    Forstner, Andreas J
    McQuillin, Andrew
    Ripke, Stephan
    Trubetskoy, Vassily
    Mattheisen, Manuel
    Wang, Yunpeng
    Coleman, Jonathan R I
    Gaspar, Héléna A
    de Leeuw, Christiaan A
    Steinberg, Stacy
    Pavlides, Jennifer M Whitehead
    Trzaskowski, Maciej
    Byrne, Enda M
    Pers, Tune H
    Holmans, Peter A
    Richards, Alexander L
    Abbott, Liam
    Agerbo, Esben
    Akil, Huda
    Albani, Diego
    Alliey-Rodriguez, Ney
    Als, Thomas D
    Anjorin, Adebayo
    Antilla, Verneri
    Awasthi, Swapnil
    Badner, Judith A
    Bækvad-Hansen, Marie
    Barchas, Jack D
    Bass, Nicholas
    Bauer, Michael
    Belliveau, Richard
    Bergen, Sarah E
    Pedersen, Carsten Bøcker
    Bøen, Erlend
    Boks, Marco P
    Boocock, James
    Budde, Monika
    Bunney, William
    Burmeister, Margit
    Bybjerg-Grauholm, Jonas
    Byerley, William
    Casas, Miquel
    Cerrato, Felecia
    Cervantes, Pablo
    Chambert, Kimberly
    Charney, Alexander W
    Chen, Danfeng
    Churchhouse, Claire
    Clarke, Toni-Kim
    Coryell, William
    Craig, David W
    Cruceanu, Cristiana
    Curtis, David
    Czerski, Piotr M
    Dale, Anders M
    de Jong, Simone
    Degenhardt, Franziska
    Del-Favero, Jurgen
    DePaulo, J Raymond
    Djurovic, Srdjan
    Dobbyn, Amanda L
    Dumont, Ashley
    Elvsåshagen, Torbjørn
    Escott-Price, Valentina
    Fan, Chun Chieh
    Fischer, Sascha B
    Flickinger, Matthew
    Foroud, Tatiana M
    Forty, Liz
    Frank, Josef
    Fraser, Christine
    Freimer, Nelson B
    Frisén, Louise
    Gade, Katrin
    Gage, Diane
    Garnham, Julie
    Giambartolomei, Claudia
    Pedersen, Marianne Giørtz
    Goldstein, Jaqueline
    Gordon, Scott D
    Gordon-Smith, Katherine
    Green, Elaine K
    Green, Melissa J
    Greenwood, Tiffany A
    Grove, Jakob
    Guan, Weihua
    Guzman-Parra, José
    Hamshere, Marian L
    Hautzinger, Martin
    Heilbronner, Urs
    Herms, Stefan
    Hipolito, Maria
    Hoffmann, Per
    Holland, Dominic
    Huckins, Laura
    Jamain, Stéphane
    Johnson, Jessica S
    Juréus, Anders
    Kandaswamy, Radhika
    Karlsson, Robert
    Kennedy, James L
    Kittel-Schneider, Sarah
    Knowles, James A
    Kogevinas, Manolis
    Koller, Anna C
    Kupka, Ralph
    Lavebratt, Catharina
    Lawrence, Jacob
    Lawson, William B
    Leber, Markus
    Lee, Phil H
    Levy, Shawn E
    Li, Jun Z
    Liu, Chunyu
    Lucae, Susanne
    Maaser, Anna
    MacIntyre, Donald J
    Mahon, Pamela B
    Maier, Wolfgang
    Martinsson, Lina
    McCarroll, Steve
    McGuffin, Peter
    McInnis, Melvin G
    McKay, James D
    Medeiros, Helena
    Medland, Sarah E
    Meng, Fan
    Milani, Lili
    Montgomery, Grant W
    Morris, Derek W
    Mühleisen, Thomas W
    Mullins, Niamh
    Nguyen, Hoang
    Nievergelt, Caroline M
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nwulia, Evaristus A
    O'Donovan, Claire
    Loohuis, Loes M Olde
    Ori, Anil P S
    Oruc, Lilijana
    Ösby, Urban
    Perlis, Roy H
    Perry, Amy
    Pfennig, Andrea
    Potash, James B
    Purcell, Shaun M
    Regeer, Eline J
    Reif, Andreas
    Reinbold, Céline S
    Rice, John P
    Rivas, Fabio
    Rivera, Margarita
    Roussos, Panos
    Ruderfer, Douglas M
    Ryu, Euijung
    Sánchez-Mora, Cristina
    Schatzberg, Alan F
    Scheftner, William A
    Schork, Nicholas J
    Shannon Weickert, Cynthia
    Shehktman, Tatyana
    Shilling, Paul D
    Sigurdsson, Engilbert
    Slaney, Claire
    Smeland, Olav B
    Sobell, Janet L
    Søholm Hansen, Christine
    Spijker, Anne T
    St Clair, David
    Steffens, Michael
    Strauss, John S
    Streit, Fabian
    Strohmaier, Jana
    Szelinger, Szabolcs
    Thompson, Robert C
    Thorgeirsson, Thorgeir E
    Treutlein, Jens
    Vedder, Helmut
    Wang, Weiqing
    Watson, Stanley J
    Weickert, Thomas W
    Witt, Stephanie H
    Xi, Simon
    Xu, Wei
    Young, Allan H
    Zandi, Peter
    Zhang, Peng
    Zöllner, Sebastian
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Agartz, Ingrid
    Alda, Martin
    Backlund, Lena
    Baune, Bernhard T
    Bellivier, Frank
    Berrettini, Wade H
    Biernacka, Joanna M
    Blackwood, Douglas H R
    Boehnke, Michael
    Børglum, Anders D
    Corvin, Aiden
    Craddock, Nicholas
    Daly, Mark J
    Dannlowski, Udo
    Esko, Tõnu
    Etain, Bruno
    Frye, Mark
    Fullerton, Janice M
    Gershon, Elliot S
    Gill, Michael
    Goes, Fernando
    Grigoroiu-Serbanescu, Maria
    Hauser, Joanna
    Hougaard, David M
    Hultman, Christina M
    Jones, Ian
    Jones, Lisa A
    Kahn, René S
    Kirov, George
    Landén, Mikael
    Leboyer, Marion
    Lewis, Cathryn M
    Li, Qingqin S
    Lissowska, Jolanta
    Martin, Nicholas G
    Mayoral, Fermin
    McElroy, Susan L
    McIntosh, Andrew M
    McMahon, Francis J
    Melle, Ingrid
    Metspalu, Andres
    Mitchell, Philip B
    Morken, Gunnar
    Mors, Ole
    Mortensen, Preben Bo
    Müller-Myhsok, Bertram
    Myers, Richard M
    Neale, Benjamin M
    Nimgaonkar, Vishwajit
    Nordentoft, Merete
    Nöthen, Markus M
    O'Donovan, Michael C
    Oedegaard, Ketil J
    Owen, Michael J
    Paciga, Sara A
    Pato, Carlos
    Pato, Michele T
    Posthuma, Danielle
    Ramos-Quiroga, Josep Antoni
    Ribasés, Marta
    Rietschel, Marcella
    Rouleau, Guy A
    Schalling, Martin
    Schofield, Peter R
    Schulze, Thomas G
    Serretti, Alessandro
    Smoller, Jordan W
    Stefansson, Hreinn
    Stefansson, Kari
    Stordal, Eystein
    Sullivan, Patrick F
    Turecki, Gustavo
    Vaaler, Arne E
    Vieta, Eduard
    Vincent, John B
    Werge, Thomas
    Nurnberger, John I
    Wray, Naomi R
    Di Florio, Arianna
    Edenberg, Howard J
    Cichon, Sven
    Ophoff, Roel A
    Scott, Laura J
    Andreassen, Ole A
    Kelsoe, John
    Sklar, Pamela
    Genome-wide association study identifies 30 loci associated with bipolar disorder2019Ingår i: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 51, nr 5, s. 793-803Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Bipolar disorder is a highly heritable psychiatric disorder. We performed a genome-wide association study (GWAS) including 20,352 cases and 31,358 controls of European descent, with follow-up analysis of 822 variants with P < 1 × 10-4 in an additional 9,412 cases and 137,760 controls. Eight of the 19 variants that were genome-wide significant (P < 5 × 10-8) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity. In the combined analysis, 30 loci were genome-wide significant, including 20 newly identified loci. The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder. These findings address key clinical questions and provide potential biological mechanisms for bipolar disorder.

  • 136. Stanciu, Ingrid
    et al.
    Larsson, Maria
    Nordin, Steven
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Goran
    Olofsson, Jonas K.
    Olfactory Impairment and Subjective Olfactory Complaints Independently Predict Conversion to Dementia: A Longitudinal, Population-Based Study2014Ingår i: Journal of the International Neuropsychological Society, ISSN 1355-6177, E-ISSN 1469-7661, Vol. 20, nr 2, s. 209-217Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We examined whether conversion to dementia can be predicted by self-reported olfactory impairment and/or by an inability to identify odors. Common forms of dementia involve an impaired sense of smell, and poor olfactory performance predicts cognitive decline among the elderly. We followed a sample of 1529 participants, who were within a normal range of overall cognitive function at baseline, over a 10-year period during which 159 were classified as having a dementia disorder. Dementia conversion was predicted from demographic variables, Mini-Mental State Examination score, and olfactory assessments. Self-reported olfactory impairment emerged as an independent predictor of dementia. After adjusting for effects of other predictors, individuals who rated their olfactory sensitivity as "worse than normal" were more likely to convert to dementia than those who reported normal olfactory sensitivity (odds ratio [OR] = 2.17; 95% confidence interval [CI] [1.40, 3.37]). Additionally, low scores on an odor identification test also predicted conversion to dementia (OR per 1 point increase = 0.89; 95% CI [0.81, 0.98]), but these two effects were additive. We suggest that assessing subjective olfactory complaints might supplement other assessments when evaluating the risk of conversion to dementia. Future studies should investigate which combination of olfactory assessments is most useful in predicting dementia conversion. (JINS, 2014, 20, 1-9)

  • 137. Stanciu, Ingrid
    et al.
    Larsson, Maria
    Nordin, Steven
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    Olofsson, Jonas K
    Olfactory impairment and subjective olfactory complaints independently predict conversion to dementia2015Ingår i: Chemical Senses, ISSN 0379-864X, E-ISSN 1464-3553, Vol. 40, nr 3, s. 260-260Artikel i tidskrift (Övrigt vetenskapligt)
  • 138.
    Sternäng, Ola
    et al.
    Department of Psychology, Stockholm University.
    Wahlin, Åke
    Department of Psychology, Stockholm University.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Sleegers, Kristel
    Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB.
    van Broeckhoven, Christine
    Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB.
    Nilsson, Lars-Göran
    Department of Psychology, Stockholm University.
    APOE and lipid level synergy effects on declarative memory functioning in adulthood2009Ingår i: European Psychologist, ISSN 1016-9040, E-ISSN 1878-531X, Vol. 14, nr 4, s. 268-278Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    This study of the general population examined interactions of the gene Apolipoprotein E (APOE) and/or lipid levels, and their effects on cognitive change. A MANCOVA model based on longitudinal data (with a 5 year follow-up) obtained from the Betula study (n = 1777; age 35–85 years) was used. The significant two-way and three-way interaction effects detected were equally frequent in tests of episodic and semantic memory. A difference in the distribution of interaction effects on episodic and semantic memory decline was also found. Men demonstrated the worst cognitive development as shown by significant two-way interaction effects on episodic memory whereas two-way interaction effects among women resulted in the worst semantic memory development. This result is discussed from the viewpoint that tests of episodic and semantic memory have different cognitive demands.This study focuses on how interaction effects of the gene APOE and vascular risk factors (such as lipid levels) affect cognitive abilities and also whether the interaction effects vary across age and sex. In this study, the main focus is on interaction effects as a phenomenon in itself.

  • 139.
    Stomby, Andreas
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin. Region Jönköping County, Jönköping, Sweden.
    Boraxbekk, Carl-Johan
    Umeå universitet, Samhällsvetenskapliga fakulteten, Enheten för demografi och åldrandeforskning (CEDAR). Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI).
    Lundquist, Anders
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI).
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI). Department of Psychology, Stockholm University, Stockholm, Sweden.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI). Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Fysiologi. Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Diagnostisk radiologi.
    Olsson, Tommy
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Higher diurnal salivary cortisol levels are related to smaller prefrontal cortex surface area in elderly men and women2016Ingår i: European Journal of Endocrinology, ISSN 0804-4643, E-ISSN 1479-683X, Vol. 175, nr 2, s. 117-126Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: Elevated cortisol levels with aging have been associated with atrophy of the hippocampus and prefrontal cortex (PFC), as well as with impaired cognitive functions in men. However, coexisting diseases have confounded many studies examining these relationships. Studies in women are lacking. Our objective was to test whether salivary cortisol levels were related to morphology of the hippocampus and the PFC, and to cognitive performance. Design: A cross-sectional study including 200 elderly (55-80 years old) men and women. Method: We used magnetic resonance imaging, tests of episodic-, semantic-, and working memory, visuospatial ability, and cortisol levels in four saliva samples collected during 1 day. Results: Area under the curve (AUC) for cortisol levels was negatively related to cortical surface area of the left anterior cingulate gyrus (caudal P < 0.001; rostral P = 0.006), right lateral orbitofrontal cortex (P = 0.004), and right rostral middle frontal gyrus (P = 0.003). In women, there was also a negative relationship with cortical surface area in the left rostral middle frontal gyrus (P = 0.006). No relationship was found between cortisol levels and hippocampal volume. Conclusion: This study suggests that the structure of the medial PFC is related to cortisol levels in both elderly women and men.

  • 140.
    Stomby, Andreas
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Boraxbekk, Carl-Johan
    Umeå universitet, Samhällsvetenskapliga fakulteten, Demografiska databasen.
    Nilsson, Lars-Göran
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI).
    Olsson, Tommy
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Higher diurnal salivary cortisol levels are related to smaller prefrontal cortex surface area in women and menManuskript (preprint) (Övrigt vetenskapligt)
  • 141. Strazisar, M
    et al.
    Cammaerts, S
    van der Ven, K
    Forero, DA
    Lenaerts, A-S
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Almeida-Souza, L
    Genovese, G
    Timmerman, V
    Liekens, A
    De Rijk, P
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Callaerts, P
    Del-Favero, J
    MIR137 variants identified in psychiatric patients affect synaptogenesis and neuronal transmission gene sets2015Ingår i: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 20, nr 4, s. 472-481Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Sequence analysis of 13 microRNA (miRNA) genes expressed in the human brain and located in genomic regions associated with schizophrenia and/or bipolar disorder, in a northern Swedish patient/control population, resulted in the discovery of two functional variants in the MIR137 gene. On the basis of their location and the allele frequency differences between patients and controls, we explored the hypothesis that the discovered variants impact the expression of the mature miRNA and consequently influence global mRNA expression affecting normal brain functioning. Using neuronal-like SH-SY5Y cells, we demonstrated significantly reduced mature miR-137 levels in the cells expressing the variant miRNA gene. Subsequent transcriptome analysis showed that the reduction in miR-137 expression led to the deregulation of gene sets involved in synaptogenesis and neuronal transmission, all implicated in psychiatric disorders. Our functional findings add to the growing data, which implicate that miR-137 has an important role in the etiology of psychiatric disorders and emphasizes its involvement in nervous system development and proper synaptic function.

  • 142.
    Sundström, A.
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nilsson, L-G.
    Cruts, M.
    Adolfsson, R
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Van Broeckhoven, C.
    Nyberg, L.
    Fatigue before and after mild head injury: pre-post injury comparisons in relation to Apolipoprotein EManuskript (Övrigt vetenskapligt)
  • 143.
    Sundström, Anna
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Marklund, Petter
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nilsson, Lars-Göran
    Department of Psychology, Stockholm University.
    Cruts, M.
    Depatrment of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Belgium.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Van Broeckhoven, C.
    Depatrment of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Belgium.
    Nyberg, Lars
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    APOE influences on neurosychological function after mild head injury: within-person comparisons2004Ingår i: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 62, nr 11, s. 1963-1966Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: To examine the relationship between neuropsychological outcome following mild head injury (MHI) and APOE genotype.

    Methods: Data from a population-based longitudinal study (n = 3,500) were used to identify 34 adults who experienced MHI during the course of the study. Their pre- and postinjury performances on a battery of nine neuropsychological tests were compared within person, and the postinjury performance was compared with that of age- and gender-matched control subjects.

    Results: The within-person comparisons showed that participants with at least oneAPOE ε4 allele (n = 11) had a significantly decreased postinjury performance on three of the tests, whereas the postinjury performance for APOE ε4-negative participants (n = 23) was unchanged. There was no significant difference in postinjury performance between participants with/without the ε4 allele, and neither group was impaired relative to controls.

    Conclusions: APOE genotype may influence the outcome following an MHI. Pre/postinjury within-person comparisons seem more sensitive than control group comparisons for detecting injury-related effects.

  • 144.
    Sundström, Anna
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nilsson, Lars-Göran
    Department of Psychology, Stockholm University.
    Cruts, M.
    Depatrment of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Belgium.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nyberg, Lars
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    van Broeckhoven, C.
    Depatrment of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Belgium.
    Fatigue before and after mild traumatic brain injury: Pre-post-injury comparisons in relation to Apolipoprotein E2007Ingår i: Brain Injury, ISSN 0269-9052, E-ISSN 1362-301X, Vol. 21, nr 10, s. 1049-1054Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Primary objective: To assess the incidence of fatigue for persons following a mild traumatic brain injury (MTBI) and to evaluate the relationship between fatigue and APOE genotype. As fatigue is often found to be influenced by anxiety, depression and sleep disturbance, these factors were also measured. Methods and procedures: Thirty-one persons who sustained a MTBI were drawn from a population-based longitudinal study. Each person who sustained a MTBI was matched by age, gender, education and APOE genotype with two non-head injury controls. Self-reported pre- and post-injury incidence of fatigue, anxiety, depression and sleep disturbance was compared within-group and between groups. Results: For the MTBI group, incidence of fatigue was almost twice as common post- than pre-injury, whereas there was no corresponding change in a non-injured control group. Within the MTBI-group, post-injury fatigue was particularly common for carriers of the APOE ε4 allele. Conclusions: Fatigue is common sequela after a MTBI and especially pronounced for carriers of the APOE ε4 allele.

  • 145.
    Sundström, Anna
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nilsson, Lars-Göran
    Department of Psychology, Stockholm University, Sweden.
    Cruts, M.
    Department of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Belgium.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Van Broeckhoven, C.
    Department of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Belgium.
    Nyberg, Lars
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Increased risk of dementia following mild head injury for carriers but not for non-carriers of the APOE ε4 allele2007Ingår i: International psychogeriatrics, ISSN 1041-6102, E-ISSN 1741-203X, Vol. 19, nr 1, s. 159-165Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The ε4 allele of apolipoprotein E (APOE) and head injury are risk factors for dementia diseases, and may act synergistically to further increase the risk. The aim of this study was to examine the association between mild head injury, APOE and dementia.

    Methods: Data were obtained from the Betula prospective population-based study of aging, memory, and health. The study included 543 participants in the age range 40–85 years, free of dementia at baseline, who were followed up within a 5-year interval. Dementia was classified using DSM-IV criteria. Information on previous head injury was obtained through screening of the participants' answers to health questionnaires at baseline and at follow-up.

    Results: Subjects with head injury but without APOE ε4 had no increased risk of dementia. Subjects with APOE ε4 had an increased risk and those with both APOE ε4 and head injury had the highest risk of dementia (odds ratio = 5.2).

    Conclusions: APOE ε4 constitutes a risk factor for dementia, mild injury in isolation does not increase the risk, but head injury in combination with the APOE ε4 leads to increased risk of dementia.

  • 146.
    Sundström, Anna
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Umeå universitet, Samhällsvetenskapliga fakulteten, Centrum för befolkningsstudier (CBS).
    Rönnlund, Michael
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Stressful life events are not associated with development of dementia2014Ingår i: International psychogeriatrics, ISSN 1041-6102, E-ISSN 1741-203X, Vol. 26, s. 147-154Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The impact of stressful life events as a risk factor of dementia diseases is inconclusive. We sought to determine whether stressful negative life events are associated with incidental dementia in a population-based study with long-term follow-up. We also tested the hypothesis that the occurrence of positive life events could mitigate or overcome the possible adverse effects of negative life events on dementia conversion.

    Methods: The study involved 2,462 dementia-free participants aged 55 years and older. Information on life events was ascertained at baseline from a comprehensive Life Event Inventory, which included 56 questions about specific life events. For each life event, the emotional impact (both positive and negative) and emotional adjustment were asked for.

    Results: During follow-up, 423 participants developed dementia; of these, 240 developed Alzheimer's disease (AD). Cox regression analysis showed no association between the total number of negative life events and the incidence of dementia when adjusted solely for age and gender (hazard ratio = 0.97, 95% CI = 0.92-1.02), or with multiple adjustments for a range of covariates (hazard ratio = 0.96, 95% CI = 0.91-1.01). Similarly, neither emotional impact nor emotional adjustment to these life events was associated with incident dementia. A separate analysis of AD did not alter the results.

    Conclusions: The result of this population-based study finds no association between negative or positive life events and dementia. Accordingly, our results reject the hypothesis that stressful life events trigger the onset of dementia diseases.

  • 147.
    Sundström, Anna
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Umeå universitet, Samhällsvetenskapliga fakulteten, Centrum för befolkningsstudier (CBS).
    Westerlund, Olle
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för nationalekonomi. Umeå universitet, Samhällsvetenskapliga fakulteten, Centrum för befolkningsstudier (CBS).
    Mousavi-Nasab, Hossein
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nilsson, Lars-Göran
    The relationship between marital and parental status and the risk of dementia2014Ingår i: International psychogeriatrics, ISSN 1041-6102, E-ISSN 1741-203X, Vol. 26, nr 5, s. 749-757Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: This study examines the association between marital and parental status and their individual and combined effect on risk of dementia diseases in a population-based longitudinal study while controlling for a range of potential confounders, including social networks and exposure to stressful negative life events. Methods: A total of 1,609 participants without dementia, aged 65 years and over, were followed for an average period of 8.6 years (SD = 4.8). During follow-up, 354 participants were diagnosed with dementia. Cox regression was used to investigate the effect of marital and parental status on risk of dementia. Results: In univariate Cox regression models (adjusted for age as time scale), widowed (hazard ratio (HR) 1.42, 95% confidence interval (CI) = 1.13-1.78), and not having children (HR 1.54, 95% CI = 1.15-2.06) were significantly associated with incident dementia. In multivariate analyses that included simultaneously marital and parental status and covariates that were found to be significant in univariate models (p < 0.10), the HR was 1.30 (95% CI = 1.01-1.66) for widowed, and 1.51 (95% CI = 1.08-2.10) for those not having children. Finally, a group of four combined factors was constructed: married parents (reference), married without children, widowed parents, and widowed without children. The combined effect revealed a 1.3 times higher risk (95% CI = 1.03-1.76) of dementia in widow parents, and a 2.2 times higher risk (95% CI = 1.36-3.60) in widowed persons without children, in relation to married parents. No significant difference was observed for those being married and without children. Conclusions: Our findings suggest that marital- and parental status are important risk factors for developing dementia, with especially increased risk in those being both widowed and without children.

  • 148. Sutrala, Smitha R
    et al.
    Goossens, Dirk
    WilliamS, Nigel M
    Heyrman, Lien
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Norton, Nadine
    Buckland, Paul R
    Del-Favero, Jurgen
    Gene copy number variation in schizophrenia2007Ingår i: Schizophrenia Research, ISSN 0920-9964, E-ISSN 1573-2509, Vol. 96, nr 1-3, s. 93-99Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The possibility that gene copy number variations play a role in the development of complex disorders is a topic of considerable interest. Recent reports have highlighted the large number of such variations that exist and that their occurrence varies considerably between populations. A recent report has suggested that copy number variations in four genes (GRIK3, EFNA5, AKAP5 and CACNG2) may be associated with schizophrenia. One problem with this area of study is the validation of high throughput methods such as comparative genomic hybridisation, as the latter inevitably generates false positives. We have used two contrasting methodologies to determine the validity of the findings reported above which if true would have major implications for the pathogenesis of schizophrenia. Samples from a UK population were tested using a method of allele quantification by DNA pooling and samples from Belgium and northern Sweden were tested using Multiplex Amplicon Quantification (MAQ). Both methods were used to test DNA samples used in the original investigation. No copy number variations were found for any of the genes in any samples. Our data suggests that more reliable methods need to be used to validate the existence of CNVs before full scale association studies are carried out.

  • 149. Szatkiewicz, Jin
    et al.
    Crowley, James J.
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Åberg, Karolina A.
    Alaerts, Maaike
    Genovese, Giulio
    McCarroll, Steven
    Del-Favero, Jurgen
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Sullivan, Patrick F.
    The genomics of major psychiatric disorders in a large pedigree from Northern Sweden2019Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 9, artikel-id 60Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We searched for genetic causes of major psychiatric disorders (bipolar disorder, schizoaffective disorder, and schizophrenia) in a large, densely affected pedigree from Northern Sweden that originated with three pairs of founders born around 1650. We applied a systematic genomic approach to the pedigree via karyotyping (N = 9), genome-wide SNP arrays (N = 418), whole-exome sequencing (N = 26), and whole-genome sequencing (N = 10). Comprehensive analysis did not identify plausible variants of strong effect. Rather, pedigree cases had significantly higher genetic risk scores compared to pedigree and community controls.

  • 150.
    Sörman, Daniel
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Ljungberg K., Jessica
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Hansson, Patrik
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap.
    Nilsson, Lars-Göran
    Psykologiska institutionen, Stockholms universitet.
    Language skills and risk of dementia: a population-based study2015Konferensbidrag (Övrigt vetenskapligt)
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