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Publications (10 of 35) Show all publications
Håglin, S., Koch, E., Schäfer Hackenhaar, F., Nyberg, L. & Kauppi, K. (2023). APOE ɛ4, but not polygenic Alzheimer’s disease risk, is related to longitudinal decrease in hippocampal brain activity in non-demented individuals. Scientific Reports, 13(1), Article ID 8433.
Open this publication in new window or tab >>APOE ɛ4, but not polygenic Alzheimer’s disease risk, is related to longitudinal decrease in hippocampal brain activity in non-demented individuals
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2023 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 13, no 1, article id 8433Article in journal (Refereed) Published
Abstract [en]

The hippocampus is affected early in Alzheimer’s disease (AD) and altered hippocampal functioning influences normal cognitive aging. Here, we used task-based functional MRI to assess if the APOE ɛ4 allele or a polygenic risk score (PRS) for AD was linked to longitudinal changes in memory-related hippocampal activation in normal aging (baseline age 50–95, n = 292; n = 182 at 4 years follow-up, subsequently non-demented for at least 2 years). Mixed-models were used to predict level and change in hippocampal activation by APOE ɛ4 status and PRS based on gene variants previously linked to AD at p ≤ 1, p < 0.05, or p < 5e−8 (excluding APOE). APOE ɛ4 and PRSp<5e−8 significantly predicted AD risk in a larger sample from the same study population (n = 1542), while PRSp≤1 predicted memory decline. APOE ɛ4 was linked to decreased hippocampal activation over time, with the most prominent effect in the posterior hippocampi, while PRS was unrelated to hippocampal activation at all p-thresholds. These results suggests a link for APOE ɛ4, but not for AD genetics in general, on functional changes of the hippocampi in normal aging.

Place, publisher, year, edition, pages
Springer Nature, 2023
National Category
Neurosciences Neurology
Identifiers
urn:nbn:se:umu:diva-209143 (URN)10.1038/s41598-023-35316-z (DOI)37225733 (PubMedID)2-s2.0-85160132679 (Scopus ID)
Funder
The Kempe Foundations, SMK-1865Swedish Research Council, 2017-03011Knut and Alice Wallenberg Foundation
Available from: 2023-06-26 Created: 2023-06-26 Last updated: 2023-06-26Bibliographically approved
Koch, E., Kauppi, K. & Chen, C.-H. (2023). Candidates for Drug Repurposing to Address the Cognitive Symptoms in Schizophrenia. Progress in Neuro-psychopharmacology and Biological Psychiatry, 20, Article ID 110637.
Open this publication in new window or tab >>Candidates for Drug Repurposing to Address the Cognitive Symptoms in Schizophrenia
2023 (English)In: Progress in Neuro-psychopharmacology and Biological Psychiatry, ISSN 0278-5846, E-ISSN 1878-4216, Vol. 20, article id 110637Article in journal (Refereed) Published
Abstract [en]

In the protein-protein interactome, we have previously identified a significant overlap between schizophrenia risk genes and genes associated with cognitive performance. Here, we further studied this overlap to identify potential candidate drugs for repurposing to treat the cognitive symptoms in schizophrenia. We first defined a cognition-related schizophrenia interactome from network propagation analyses, and identified drugs known to target more than one protein within this network. Thereafter, we used gene expression data to further select drugs that could counteract schizophrenia-associated gene expression perturbations. Additionally, we stratified these analyses by sex to identify sex-specific pharmacological treatment options for the cognitive symptoms in schizophrenia. After excluding drugs contraindicated in schizophrenia, we identified 12 drug repurposing candidates, most of which have anti-inflammatory and neuroprotective effects. Sex-stratified analyses showed that out of these 12 drugs, four were identified in females only, three were identified in males only, and five were identified in both sexes. Based on our bioinformatics analyses of disease genetics, we suggest 12 candidate drugs that warrant further examination for repurposing to treat the cognitive symptoms in schizophrenia, and suggest that these symptoms could be addressed by sex-specific pharmacological treatment options.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Cognition, Genetics, Network medicine, Protein-protein interactome, Schizophrenia, Sex differences
National Category
Medical Genetics
Identifiers
urn:nbn:se:umu:diva-193658 (URN)10.1016/j.pnpbp.2022.110637 (DOI)000885857500001 ()36099967 (PubMedID)2-s2.0-85139721645 (Scopus ID)
Funder
NIH (National Institutes of Health), R56AG061163NIH (National Institutes of Health), R01MH118281Swedish Research Council, 2017-03011
Note

Originally included in thesis in manuscript form. 

Available from: 2022-04-10 Created: 2022-04-10 Last updated: 2023-01-12Bibliographically approved
Supiyev, A., Karlsson, R., Wang, Y., Koch, E., Hägg, S. & Kauppi, K. (2023). Independent role of Alzheimer's disease genetics and C-reactive protein on cognitive ability in aging. Neurobiology of Aging, 126, 103-112
Open this publication in new window or tab >>Independent role of Alzheimer's disease genetics and C-reactive protein on cognitive ability in aging
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2023 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 126, p. 103-112Article in journal (Refereed) Published
Abstract [en]

Apolipoprotein E (APOE) ε4, the strongest genetic risk factor for late onset Alzheimer's disease (LOAD), has been associated with cognitive decline independent from AD pathology, but the role for other LOAD risk genes in normal cognitive aging is less studied. We examined the effect of APOE ε4 and several different polygenic risk scores (PRS) for LOAD on cognitive level and decline in aging, using longitudinal data from the UK Biobank. While PRS-LOAD including all variants (except APOE) predicted cognitive level, APOE ε4 and PRS-LOAD based on 17 non-APOE gene variants with strong association to AD (p < 5e-8) predicted age-related decline in verbal numeric reasoning. The effect on decline were partly driven by 4 variants involved in the immune system. Those variants also predicted serum levels of the inflammatory marker C-reactive protein (CRP), but CRP did not mediate the effect on decline. Those findings suggest genetic variations in immune functions play a role in aspects of cognitive aging that may be independent of LOAD pathology as well as systemic inflammation measured by CRP.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Alzheimer's disease, APOE, Cognitive aging, Pathway-based PRS-LOAD, Polygenic risk scores, Serum CRP
National Category
Geriatrics
Identifiers
urn:nbn:se:umu:diva-206355 (URN)10.1016/j.neurobiolaging.2023.02.006 (DOI)000961467100001 ()36965205 (PubMedID)2-s2.0-85150886818 (Scopus ID)
Funder
Swedish Research Council, 2018-05973Swedish Research Council, 2015-03255Swedish Research Council, 2019- 01272Swedish Research Council, 2020-06101The Karolinska Institutet's Research FoundationKonung Gustaf V:s och Drottning Victorias FrimurarestiftelseSwedish Research Council, 2017-03011The Karolinska Institutet's Research Foundation, 2020-02260
Available from: 2023-04-26 Created: 2023-04-26 Last updated: 2023-04-26Bibliographically approved
Koch, E., Johnell, K. & Kauppi, K. (2023). Longitudinal effects of using and discontinuing central nervous system medications on cognitive functioning. Pharmacoepidemiology and Drug Safety, 32(4), 446-454
Open this publication in new window or tab >>Longitudinal effects of using and discontinuing central nervous system medications on cognitive functioning
2023 (English)In: Pharmacoepidemiology and Drug Safety, ISSN 1053-8569, E-ISSN 1099-1557, Vol. 32, no 4, p. 446-454Article in journal (Refereed) Published
Abstract [en]

Purpose: To investigate the longitudinal effect of using and discontinuing central nervous system (CNS) medications on cognitive performance.

Methods: Using longitudinal cognitive data from population representative adults aged 25–100 years (N = 2188) from four test waves 5 years apart, we investigated both the link between use of CNS medications (opioids, anxiolytics, hypnotics and sedatives) on cognitive task performance (episodic memory, semantic memory, visuospatial ability) across 15 years, and the effect of discontinuing these medications in linear mixed effects models.

Results: We found that opioid use was associated with decline in visuospatial ability whereas using anxiolytics, hypnotics and sedatives was not associated with cognitive decline over 15 years. A link between drug discontinuation and cognitive improvement was seen for opioids as well as for anxiolytics, hypnotics and sedatives.

Conclusions: Although our results may be confounded by subjacent conditions, they suggest that long-term use of CNS medications may have domain-specific negative effects on cognitive performance over time, whereas the discontinuation of these medications may partly reverse these effects. These results open up for future studies that address subjacent conditions on cognition to develop a more complete understanding of the cognitive effects of CNS medications.

Place, publisher, year, edition, pages
John Wiley & Sons, 2023
Keywords
CNS drugs, cognitive decline, cognitive function, drug discontinuation
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:umu:diva-201345 (URN)10.1002/pds.5569 (DOI)000889268200001 ()36357173 (PubMedID)2-s2.0-85142277047 (Scopus ID)
Funder
Swedish Research Council, 2017–03011
Available from: 2022-12-14 Created: 2022-12-14 Last updated: 2023-07-13Bibliographically approved
Schäfer Hackenhaar, F., Josefsson, M., Nordin Adolfsson, A., Landfors, M., Kauppi, K., Porter, T., . . . the Australian Imaging Biomarkers and Lifestyle Study, . (2023). Sixteen-year longitudinal evaluation of blood-based DNA methylation biomarkers for early prediction of Alzheimer’s disease. Journal of Alzheimer's Disease, 94(4), 1443-1464
Open this publication in new window or tab >>Sixteen-year longitudinal evaluation of blood-based DNA methylation biomarkers for early prediction of Alzheimer’s disease
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2023 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 94, no 4, p. 1443-1464Article in journal (Refereed) Published
Abstract [en]

Background: DNA methylation (DNAm), an epigenetic mark reflecting both inherited and environmental influences, hasshown promise for Alzheimer’s disease (AD) prediction.Objective: Testing long-term predictive ability (>15 years) of existing DNAm-based epigenetic age acceleration (EAA)measures and identifying novel early blood-based DNAm AD-prediction biomarkers.

Methods: EAA measures calculated from Illumina EPIC data from blood were tested with linear mixed-effects models(LMMs) in a longitudinal case-control sample (50 late-onset AD cases; 51 matched controls) with prospective data up to 16years before clinical onset, and post-onset follow-up. NovelDNAmbiomarkers were generated with epigenome-wide LMMs,and Sparse Partial Least Squares Discriminant Analysis applied at pre- (10–16 years), and post-AD-onset time-points.

Results: EAA did not differentiate cases from controls during the follow-up time (p > 0.05). Three new DNA biomarkersshowed in-sample predictive ability on average 8 years pre-onset, after adjustment for age, sex, and white blood cell proportions(p-values: 0.022-<0.00001). Our longitudinally-derived panel replicated nominally (p = 0.012) in an external cohort (n = 146cases, 324 controls). However, its effect size and discriminatory accuracy were limited compared to APOE 4-carriership(OR = 1.38 per 1 SD DNAmscore increase versus OR= 13.58 for 4-allele carriage; AUCs = 77.2% versus 87.0%). Literaturereview showed low overlap (n = 4) across 3275 AD-associated CpGs from 8 published studies, and no overlap with ouridentified CpGs.

Conclusion: The limited predictive value of EAA for AD extends prior findings by considering a longer follow-up time, andwith appropriate control for age, sex, APOE, and blood-cell proportions. Results also highlight challenges with replicatingdiscriminatory or predictive CpGs across studies.

Place, publisher, year, edition, pages
IOS Press, 2023
Keywords
Alzheimer’s disease, biomarkers, DNA methylation, epigenomics, longitudinal studies
National Category
Other Basic Medicine
Identifiers
urn:nbn:se:umu:diva-214007 (URN)10.3233/jad-230039 (DOI)37393498 (PubMedID)2-s2.0-85168428453 (Scopus ID)
Funder
Swedish Research Council, 2018-01729The Kempe Foundations, JCK-1922.1
Available from: 2023-09-02 Created: 2023-09-02 Last updated: 2024-04-08Bibliographically approved
Koch, E., Nyberg, L., Lundquist, A. & Kauppi, K. (2022). Polygenic Risk for Schizophrenia Has Sex-Specific Effects on Brain Activity during Memory Processing in Healthy Individuals. Genes, 13(3), Article ID 412.
Open this publication in new window or tab >>Polygenic Risk for Schizophrenia Has Sex-Specific Effects on Brain Activity during Memory Processing in Healthy Individuals
2022 (English)In: Genes, ISSN 2073-4425, E-ISSN 2073-4425, Vol. 13, no 3, article id 412Article in journal (Refereed) Published
Abstract [en]

Genetic risk for schizophrenia has a negative impact on memory and other cognitive abilities in unaffected individuals, and it was recently shown that this effect is specific to males. Using functional MRI, we investigated the effect of a polygenic risk score (PRS) for schizophrenia on brain activation during working memory and episodic memory in 351 unaffected participants (167 males and 184 females, 25–95 years), and specifically tested if any effect of PRS on brain activation is sex-specific. Schizophrenia PRS was significantly associated with decreased brain activation in the left dorsolateral prefrontal cortex (DLPFC) during working-memory manipulation and in the bilateral superior parietal lobule (SPL) during episodic-memory encoding and retrieval. A significant interaction effect between sex and PRS was seen in the bilateral SPL during episodic-memory encoding and retrieval, and sex-stratified analyses showed that the effect of PRS on SPL activation was male-specific. These results confirm previous findings of DLPFC inefficiency in schizophrenia, and highlight the SPL as another important genetic intermediate phenotype of the disease. The observed sex differences suggest that the previously shown male-specific effect of schizophrenia PRS on cognition translates into an additional corresponding effect on brain functioning.

Place, publisher, year, edition, pages
MDPI, 2022
Keywords
memory processing, brain activity, fMRI, polygenic risk, schizophrenia, sex differences, dorsolateral prefrontal cortex, superior parietal lobule
National Category
Genetics
Identifiers
urn:nbn:se:umu:diva-192804 (URN)10.3390/genes13030412 (DOI)000775272700001 ()2-s2.0-85125670255 (Scopus ID)
Funder
Swedish Research Council, 2017-03011Swedish Research Council, 2017-03011
Available from: 2022-02-28 Created: 2022-02-28 Last updated: 2023-09-05Bibliographically approved
Koch, E., Nyberg, L., Lundquist, A., Pudas, S., Adolfsson, R. & Kauppi, K. (2021). Sex-specific effects of polygenic risk for schizophrenia on lifespan cognitive functioning in healthy individuals. Translational Psychiatry, 11(1), Article ID 520.
Open this publication in new window or tab >>Sex-specific effects of polygenic risk for schizophrenia on lifespan cognitive functioning in healthy individuals
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2021 (English)In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 11, no 1, article id 520Article in journal (Refereed) Published
Abstract [en]

Polygenic risk for schizophrenia has been associated with lower cognitive ability and age-related cognitive change in healthy individuals. Despite well-established neuropsychological sex differences in schizophrenia patients, genetic studies on sex differences in schizophrenia in relation to cognitive phenotypes are scarce. Here, we investigated whether the effect of a polygenic risk score (PRS) for schizophrenia on childhood, midlife, and late-life cognitive function in healthy individuals is modified by sex, and if PRS is linked to accelerated cognitive decline. Using a longitudinal data set from healthy individuals aged 25–100 years (N = 1459) spanning a 25-year period, we found that PRS was associated with lower cognitive ability (episodic memory, semantic memory, visuospatial ability), but not with accelerated cognitive decline. A significant interaction effect between sex and PRS was seen on cognitive task performance, and sex-stratified analyses showed that the effect of PRS was male-specific. In a sub-sample, we observed a male-specific effect of the PRS on school performance at age 12 (N = 496). Our findings of sex-specific effects of schizophrenia genetics on cognitive functioning across the lifespan indicate that the effects of underlying disease genetics on cognitive functioning is dependent on biological processes that differ between the sexes.

Place, publisher, year, edition, pages
Springer Nature, 2021
Keywords
Biological Psychiatry, Cellular and Molecular Neuroscience, Psychiatry and Mental health
National Category
Psychiatry
Identifiers
urn:nbn:se:umu:diva-189060 (URN)10.1038/s41398-021-01649-4 (DOI)000706129100002 ()34635642 (PubMedID)2-s2.0-85116814483 (Scopus ID)
Funder
The Royal Swedish Academy of Sciences, AS2015-0004Swedish Research Council, 2017-03011
Available from: 2021-11-03 Created: 2021-11-03 Last updated: 2024-04-08Bibliographically approved
Pudas, S., Josefsson, M., Nordin Adolfsson, A., Landfors, M., Kauppi, K., Veng-Taasti, L. M., . . . Degerman, S. (2021). Short leukocyte telomeres, but not telomere attrition rates, predict memory decline in the 20-year longitudinal Betula study. The journals of gerontology. Series A, Biological sciences and medical sciences, 76(6), 955-963
Open this publication in new window or tab >>Short leukocyte telomeres, but not telomere attrition rates, predict memory decline in the 20-year longitudinal Betula study
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2021 (English)In: The journals of gerontology. Series A, Biological sciences and medical sciences, ISSN 1079-5006, E-ISSN 1758-535X, Vol. 76, no 6, p. 955-963Article in journal (Refereed) Published
Abstract [en]

Leukocyte telomere length (LTL) is a proposed biomarker for aging-related disorders, including cognitive decline and dementia. Long-term longitudinal studies measuring intra-individual changes in both LTL and cognitive outcomes are scarce, precluding strong conclusions about a potential aging-related relationship between LTL shortening and cognitive decline. This study investigated associations between baseline levels and longitudinal changes in LTL and memory performance across an up to 20-year follow-up in 880 dementia-free participants from a population-based study (mean baseline age: 56.8 years, range: 40–80; 52% female). Shorter baseline LTL significantly predicted subsequent memory decline (r = .34, 95% confidence interval: 0.06, 0.82), controlling for age, sex, and other relevant covariates. No significant associations were however observed between intra-individual changes in LTL and memory, neither concurrently nor with a 5-year time-lag between LTL shortening and memory decline. These results support the notion of short LTL as a predictive factor for aging-related memory decline, but suggest that LTL dynamics in adulthood and older age may be less informative of cognitive outcomes in aging. Furthermore, the results highlight the importance of long-term longitudinal evaluation of outcomes in biomarker research.

Place, publisher, year, edition, pages
Oxford University Press, 2021
Keywords
Cognitive aging, Leukocyte telomere length, Longitudinal, Memory, Population-based
National Category
Gerontology, specialising in Medical and Health Sciences Geriatrics Neurosciences
Research subject
medical behavioral science; Geriatrics; Psychology
Identifiers
urn:nbn:se:umu:diva-181484 (URN)10.1093/gerona/glaa322 (DOI)000659456700002 ()33367599 (PubMedID)2-s2.0-85107088699 (Scopus ID)
Funder
Swedish Research Council, 2018-01729Region Västerbotten, RV-735451, RV-453141, RV-225461
Available from: 2021-03-13 Created: 2021-03-13 Last updated: 2024-04-08Bibliographically approved
Schäfer Hackenhaar, F., Josefsson, M., Nordin Adolfsson, A., Landfors, M., Kauppi, K., Hultdin, M., . . . Pudas, S. (2021). Short leukocyte telomeres predict 25-year Alzheimer's disease incidence in non-APOE ε4-carriers. Alzheimer's Research & Therapy, 13, Article ID 130.
Open this publication in new window or tab >>Short leukocyte telomeres predict 25-year Alzheimer's disease incidence in non-APOE ε4-carriers
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2021 (English)In: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 13, article id 130Article in journal (Refereed) Published
Abstract [en]

Background: Leukocyte telomere length (LTL) has been shown to predict Alzheimer’s disease (AD), albeit inconsistently. Failing to account for the competing risks between AD, other dementia types, and mortality, can be an explanation for the inconsistent findings in previous time-to-event analyses. Furthermore, previous studies indicate that the association between LTL and AD is non-linear and may differ depending on apolipoprotein E (APOE) ε4 allele carriage, the strongest genetic AD predictor.

Methods: We analyzed whether baseline LTL in interaction with APOE ε4 predicts AD, by following 1306 initially non-demented subjects for 25 years. Gender- and age-residualized LTL (rLTL) was categorized into tertiles of short, medium, and long rLTLs. Two complementary time-to-event models that account for competing risks were used; the Fine-Gray model to estimate the association between the rLTL tertiles and the cumulative incidence of AD, and the cause-specific hazard model to assess whether the cause-specific risk of AD differed between the rLTL groups. Vascular dementia and death were considered competing risk events. Models were adjusted for baseline lifestyle-related risk factors, gender, age, and non-proportional hazards.

Results: After follow-up, 149 were diagnosed with AD, 96 were diagnosed with vascular dementia, 465 died without dementia, and 596 remained healthy. Baseline rLTL and other covariates were assessed on average 8 years before AD onset (range 1–24). APOE ε4-carriers had significantly increased incidence of AD, as well as increased cause-specific AD risk. A significant rLTL-APOE interaction indicated that short rLTL at baseline was significantly associated with an increased incidence of AD among non-APOE ε4-carriers (subdistribution hazard ratio = 3.24, CI 1.404–7.462, P = 0.005), as well as borderline associated with increased cause-specific risk of AD (cause-specific hazard ratio = 1.67, CI 0.947–2.964, P = 0.07). Among APOE ε4-carriers, short or long rLTLs were not significantly associated with AD incidence, nor with the cause-specific risk of AD.

Conclusions: Our findings from two complementary competing risk time-to-event models indicate that short rLTL may be a valuable predictor of the AD incidence in non-APOE ε4-carriers, on average 8 years before AD onset. More generally, the findings highlight the importance of accounting for competing risks, as well as the APOE status of participants in AD biomarker research.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2021
Keywords
Leukocyte telomere length, Dementia, Risk factors, Time-to-event analysis, Competing risks, Vascular dementia, Death
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-186769 (URN)10.1186/s13195-021-00871-y (DOI)000673978800001 ()34266503 (PubMedID)2-s2.0-85110170246 (Scopus ID)
Note

Correction: Hackenhaar, F.S., Josefsson, M., Adolfsson, A.N. et al. Correction: Short leukocyte telomeres predict 25-year Alzheimer’s disease incidence in non-APOE ε4-carriers. Alz Res Therapy 16, 39 (2024). DOI: 10.1186/s13195-024-01388-w

Available from: 2021-08-20 Created: 2021-08-20 Last updated: 2024-04-08Bibliographically approved
Nyberg, L., Boraxbekk, C.-J., Eriksson Sörman, D., Hansson, P., Herlitz, A., Kauppi, K., . . . Adolfsson, R. (2020). Biological and environmental predictors of heterogeneity in neurocognitive ageing: Evidence from Betula and other longitudinal studies. Ageing Research Reviews, 64, Article ID 101184.
Open this publication in new window or tab >>Biological and environmental predictors of heterogeneity in neurocognitive ageing: Evidence from Betula and other longitudinal studies
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2020 (English)In: Ageing Research Reviews, ISSN 1568-1637, E-ISSN 1872-9649, Vol. 64, article id 101184Article in journal (Refereed) Published
Abstract [en]

Individual differences in cognitive performance increase with advancing age, reflecting marked cognitive changes in some individuals along with little or no change in others. Genetic and lifestyle factors are assumed to influence cognitive performance in ageing by affecting the magnitude and extent of age-related brain changes (i.e., brain maintenance or atrophy), as well as the ability to recruit compensatory processes. The purpose of this review is to present findings from the Betula study and other longitudinal studies, with a focus on clarifying the role of key biological and environmental factors assumed to underlie individual differences in brain and cognitive ageing. We discuss the vital importance of sampling, analytic methods, consideration of non-ignorable dropout, and related issues for valid conclusions on factors that influence healthy neurocognitive ageing.

Place, publisher, year, edition, pages
Elsevier, 2020
Keywords
ageing, memory, longitudinal, brain, genetics, lifestyle, brain maintenance, cognitive reserve
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-176224 (URN)10.1016/j.arr.2020.101184 (DOI)000595935300003 ()32992046 (PubMedID)2-s2.0-85092710312 (Scopus ID)
Funder
Knut and Alice Wallenberg Foundation, KAW-scholarEU, Horizon 2020, 732592EU, Horizon 2020, H2020-SC1-2016-2017EU, Horizon 2020, H2020-SC1-2016-RTDSwedish Research Council, 2017- 00639Region VästerbottenThe Dementia Association - The National Association for the Rights of the DementedKnut and Alice Wallenberg Foundation, KAW 2014.0205Swedish Research Council, 2015–02199Swedish Research Council, 2017- 03011Swedish Research Council, (2018-01729Swedish Research Council Formas, 942–2015-1099
Available from: 2020-10-22 Created: 2020-10-22 Last updated: 2024-04-25Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-4908-341X

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