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Publications (10 of 72) Show all publications
Boen, R., Kaufmann, T., van der Meer, D., Frei, O., Agartz, I., Ames, D., . . . Sønderby, I. E. (2024). Beyond the global brain differences: intraindividual variability differences in 1q21.1 distal and 15q11.2 bp1-bp2 deletion carriers. Biological Psychiatry, 95(2), 147-160
Open this publication in new window or tab >>Beyond the global brain differences: intraindividual variability differences in 1q21.1 distal and 15q11.2 bp1-bp2 deletion carriers
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2024 (English)In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 95, no 2, p. 147-160Article in journal (Refereed) Published
Abstract [en]

Background: Carriers of the 1q21.1 distal and 15q11.2 BP1-BP2 copy number variants exhibit regional and global brain differences compared with noncarriers. However, interpreting regional differences is challenging if a global difference drives the regional brain differences. Intraindividual variability measures can be used to test for regional differences beyond global differences in brain structure.

Methods: Magnetic resonance imaging data were used to obtain regional brain values for 1q21.1 distal deletion (n = 30) and duplication (n = 27) and 15q11.2 BP1-BP2 deletion (n = 170) and duplication (n = 243) carriers and matched noncarriers (n = 2350). Regional intra-deviation scores, i.e., the standardized difference between an individual's regional difference and global difference, were used to test for regional differences that diverge from the global difference.

Results: For the 1q21.1 distal deletion carriers, cortical surface area for regions in the medial visual cortex, posterior cingulate, and temporal pole differed less and regions in the prefrontal and superior temporal cortex differed more than the global difference in cortical surface area. For the 15q11.2 BP1-BP2 deletion carriers, cortical thickness in regions in the medial visual cortex, auditory cortex, and temporal pole differed less and the prefrontal and somatosensory cortex differed more than the global difference in cortical thickness.

Conclusions: We find evidence for regional effects beyond differences in global brain measures in 1q21.1 distal and 15q11.2 BP1-BP2 copy number variants. The results provide new insight into brain profiling of the 1q21.1 distal and 15q11.2 BP1-BP2 copy number variants, with the potential to increase understanding of the mechanisms involved in altered neurodevelopment.

Keywords
15q11.2 BP1-BP2, 1q21.1 distal, Brain structure, Copy number variants, Intraindividual variability, Magnetic resonance imaging
National Category
Psychiatry
Identifiers
urn:nbn:se:umu:diva-218106 (URN)10.1016/j.biopsych.2023.08.018 (DOI)37661008 (PubMedID)2-s2.0-85178151168 (Scopus ID)
Funder
EU, Horizon 2020NIH (National Institutes of Health)Knut and Alice Wallenberg FoundationThe Research Council of Norway
Available from: 2023-12-15 Created: 2023-12-15 Last updated: 2023-12-15Bibliographically approved
Roe, J. M., Vidal-Piñeiro, D., Sørensen, Ø., Grydeland, H., Leonardsen, E. H., Iakunchykova, O., . . . Wang, Y. (2024). Brain change trajectories in healthy adults correlate with Alzheimer’s related genetic variation and memory decline across life. Nature Communications, 15(1), Article ID 10651.
Open this publication in new window or tab >>Brain change trajectories in healthy adults correlate with Alzheimer’s related genetic variation and memory decline across life
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2024 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 15, no 1, article id 10651Article in journal (Refereed) Published
Abstract [en]

Throughout adulthood and ageing our brains undergo structural loss in an average pattern resembling faster atrophy in Alzheimer’s disease (AD). Using a longitudinal adult lifespan sample (aged 30-89; 2–7 timepoints) and four polygenic scores for AD, we show that change in AD-sensitive brain features correlates with genetic AD-risk and memory decline in healthy adults. We first show genetic risk links with more brain loss than expected for age in early Braak regions, and find this extends beyond APOE genotype. Next, we run machine learning on AD-control data from the Alzheimer’s Disease Neuroimaging Initiative using brain change trajectories conditioned on age, to identify AD-sensitive features and model their change in healthy adults. Genetic AD-risk linked with multivariate change across many AD-sensitive features, and we show most individuals over age ~50 are on an accelerated trajectory of brain loss in AD-sensitive regions. Finally, high genetic risk adults with elevated brain change showed more memory decline through adulthood, compared to high genetic risk adults with less brain change. Our findings suggest quantitative AD risk factors are detectable in healthy individuals, via a shared pattern of ageing- and AD-related neurodegeneration that occurs along a continuum and tracks memory decline through adulthood.

Place, publisher, year, edition, pages
Nature Publishing Group, 2024
National Category
Neurosciences Neurology
Identifiers
urn:nbn:se:umu:diva-233465 (URN)10.1038/s41467-024-53548-z (DOI)001380143300004 ()39690174 (PubMedID)2-s2.0-85212711594 (Scopus ID)
Funder
EU, European Research Council, 283634EU, European Research Council, 725025EU, European Research Council, 313440The Research Council of Norway, 249931EU, Horizon 2020, 732592Knut and Alice Wallenberg Foundation
Available from: 2025-01-09 Created: 2025-01-09 Last updated: 2025-01-09Bibliographically approved
Stålnacke, M., Eriksson, J., Salami, A., Andersson, M., Nyberg, L. & Sjöberg, R. L. (2024). Functional connectivity of the sensorimotor network before and after surgery in the supplementary motor area. Neuropsychologia, 204, Article ID 109004.
Open this publication in new window or tab >>Functional connectivity of the sensorimotor network before and after surgery in the supplementary motor area
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2024 (English)In: Neuropsychologia, ISSN 0028-3932, E-ISSN 1873-3514, Vol. 204, article id 109004Article in journal (Refereed) Published
Abstract [en]

After resective glioma surgery in the Supplementary Motor Area (SMA), patients often experience a transient disturbance of the ability to initiate speech and voluntary motor actions, known as the SMA syndrome (SMAS). It has been proposed that enhanced interhemispheric functional connectivity (FC) within the sensorimotor system may serve as a potential mechanism for recovery, enabling the non-resected SMA to assume the function of the resected region. The purpose of the present study was to investigate the extent to which changes in FC can be observed in patients after resolution of the SMAS.

Eight patients underwent resection of left SMA due to suspected gliomas, resulting in various levels of the SMA syndrome. Resting-state functional MR images were acquired prior to the surgery and after resolution of the syndrome.

At the group level we found an increased connectivity between the unaffected (right) SMA and the primary motor cortex on the same side following surgery. However, no significant increase in interhemispheric connectivity was observed.

These findings challenge the prevailing notion that increased interhemispheric FC serves as the only mechanism underlying recovery from SMA syndrome and suggest the presence of one or more alternative mechanisms.

Place, publisher, year, edition, pages
Elsevier, 2024
Keywords
Glioma, Supplementary motor area, SMA, Interhemispheric connectivity, Functional imaging
National Category
Neurosciences
Research subject
Neurosurgery
Identifiers
urn:nbn:se:umu:diva-206849 (URN)10.1016/j.neuropsychologia.2024.109004 (DOI)001325130500001 ()39299453 (PubMedID)2-s2.0-85204550323 (Scopus ID)
Funder
Region VästerbottenSjöberg FoundationCancerforskningsfonden i Norrland
Available from: 2023-04-18 Created: 2023-04-18 Last updated: 2024-10-14Bibliographically approved
Karalija, N., Papenberg, G., Johansson, J., Wåhlin, A., Salami, A., Andersson, M., . . . Nyberg, L. (2024). Longitudinal support for the correlative triad among aging, dopamine D2-like receptor loss, and memory decline. Neurobiology of Aging, 136, 125-132
Open this publication in new window or tab >>Longitudinal support for the correlative triad among aging, dopamine D2-like receptor loss, and memory decline
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2024 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 136, p. 125-132Article in journal (Refereed) Published
Abstract [en]

Dopamine decline is suggested to underlie aging-related cognitive decline, but longitudinal examinations of this link are currently missing. We analyzed 5-year longitudinal data for a sample of healthy, older adults (baseline: n = 181, age: 64–68 years; 5-year follow-up: n = 129) who underwent positron emission tomography with 11C-raclopride to assess dopamine D2-like receptor (DRD2) availability, magnetic resonance imaging to evaluate structural brain measures, and cognitive tests. Health, lifestyle, and genetic data were also collected. A data-driven approach (k-means cluster analysis) identified groups that differed maximally in DRD2 decline rates in age-sensitive brain regions. One group (n = 47) had DRD2 decline exclusively in the caudate and no cognitive decline. A second group (n = 72) had more wide-ranged DRD2 decline in putamen and nucleus accumbens and also in extrastriatal regions. The latter group showed significant 5-year working memory decline that correlated with putamen DRD2 decline, along with higher dementia and cardiovascular risk and a faster biological pace of aging. Taken together, for individuals with more extensive DRD2 decline, dopamine decline is associated with memory decline in aging.

Keywords
11C-raclopride, Aging, Dopamine D2-like receptor, Longitudinal, Magnetic resonance imaging, Positron emission tomography, Working memory
National Category
Geriatrics
Identifiers
urn:nbn:se:umu:diva-221540 (URN)10.1016/j.neurobiolaging.2024.02.001 (DOI)38359585 (PubMedID)2-s2.0-85185304249 (Scopus ID)
Funder
Swedish Research Council, 421-2012-648Swedish Research Council, 2017-02217Swedish Research Council, 2022-01804Umeå UniversityKnut and Alice Wallenberg Foundation, 2015.0277Jonas and Christina af Jochnick FoundationAlzheimerfonden, AF-967710Riksbankens Jubileumsfond, P20-0779Region Västerbotten
Available from: 2024-03-15 Created: 2024-03-15 Last updated: 2024-03-15Bibliographically approved
Papenberg, G., Karalija, N., Johansson, J., Andersson, M., Axelsson, J., Riklund, K., . . . Bäckman, L. (2024). The influence of hippocampal dopamine D2 receptor losses on episodic-memory decline across 5 years is moderated by BDNF and KIBRA polymorphisms. Cortex, 176, 53-61
Open this publication in new window or tab >>The influence of hippocampal dopamine D2 receptor losses on episodic-memory decline across 5 years is moderated by BDNF and KIBRA polymorphisms
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2024 (English)In: Cortex, ISSN 0010-9452, E-ISSN 1973-8102, Vol. 176, p. 53-61Article in journal (Refereed) Published
Abstract [en]

Losses in dopamine (DA) functioning may contribute to aging-related decline in cognition. Hippocampal DA is necessary for successful episodic memory formation. Previously, we reported that higher DA D2 receptor (D2DR) availability in hippocampus is beneficial for episodic memory only in older carriers of more advantageous genotypes of well-established plasticity-related genetic variations, the brain-derived neurotrophic factor (BDNF, rs6265) and the kidney and brain expressed protein (KIBRA, rs17070145) polymorphisms. Extending our observations to the longitudinal level, the current data show that individuals with one or no beneficial BDNF and KIBRA genotype (n = 80) decline more in episodic memory across five years, without any contribution of losses in hippocampal D2DR availability to memory decline. Although carriers of two beneficial genotypes (n = 39) did not decline overall in episodic memory, losses of hippocampal D2DR availability were predictive of episodic-memory decline among these individuals. Our findings have implications for interventions targeting DA modulation to enhance episodic memory in aging, which may not benefit all older individuals.

Place, publisher, year, edition, pages
Elsevier, 2024
Keywords
BNDF, Dopamine D2 receptors, Episodic memory, Inter-individual differences, KIBRA, Longitudinal, [11C]raclopride
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-224932 (URN)10.1016/j.cortex.2024.01.014 (DOI)38749085 (PubMedID)2-s2.0-85192831317 (Scopus ID)
Funder
Swedish Research CouncilRegion VästerbottenKnut and Alice Wallenberg FoundationTorsten Söderbergs stiftelseRagnar Söderbergs stiftelseJonas and Christina af Jochnick FoundationThe Swedish Brain FoundationRegion VästerbottenMax Planck SocietyGerman Research Foundation (DFG)
Available from: 2024-05-30 Created: 2024-05-30 Last updated: 2024-05-30Bibliographically approved
Johansson, J., Nordin, K., Pedersen, R., Karalija, N., Papenberg, G., Andersson, M., . . . Salami, A. (2023). Biphasic patterns of age-related differences in dopamine D1 receptors across the adult lifespan. Cell Reports, 42(9), Article ID 113107.
Open this publication in new window or tab >>Biphasic patterns of age-related differences in dopamine D1 receptors across the adult lifespan
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2023 (English)In: Cell Reports, E-ISSN 2211-1247, Vol. 42, no 9, article id 113107Article in journal (Refereed) Published
Abstract [en]

Age-related alterations in D1-like dopamine receptor (D1DR) have distinct implications for human cognition and behavior during development and aging, but the timing of these periods remains undefined. Enabled by a large sample of in vivo assessments (n = 180, age 20 to 80 years of age, 50% female), we discover that age-related D1DR differences pivot at approximately 40 years of age in several brain regions. Focusing on the most age-sensitive dopamine-rich region, we observe opposing pre- and post-forties interrelations among caudate D1DR, cortico-striatal functional connectivity, and memory. Finally, particularly caudate D1DR differences in midlife and beyond, but not in early adulthood, associate with manifestation of white matter lesions. The present results support a model by which excessive dopamine modulation in early adulthood and insufficient modulation in aging are deleterious to brain function and cognition, thus challenging a prevailing view of monotonic D1DR function across the adult lifespan.

Keywords
aging, cognition, CP: Neuroscience, dopamine D1, functional connectivity, neuromodulation, protracted development
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-214414 (URN)10.1016/j.celrep.2023.113107 (DOI)2-s2.0-85169884676 (Scopus ID)
Funder
Swedish Research Council, 2016-01936Knut and Alice Wallenberg FoundationRiksbankens Jubileumsfond
Available from: 2023-09-18 Created: 2023-09-18 Last updated: 2024-07-02Bibliographically approved
Andersson, P., Samrani, G., Andersson, M. & Persson, J. (2023). Hippocampal subfield volumes contribute to working memory interference control in aging: evidence from longitudinal associations over 5 years. Neuroimage: Reports, 3(4), Article ID 100189.
Open this publication in new window or tab >>Hippocampal subfield volumes contribute to working memory interference control in aging: evidence from longitudinal associations over 5 years
2023 (English)In: Neuroimage: Reports, E-ISSN 2666-9560, Vol. 3, no 4, article id 100189Article in journal (Refereed) Published
Abstract [en]

In memory, familiar but no longer relevant information may disrupt encoding and retrieval of to-be-learned information. While it has been demonstrated that the ability to resolve proactive interference (PI) in working memory (WM) is reduced in aging, the neuroanatomical components of this decline have yet to be determined. Hippocampal (HC) involvement in age-related decline in control of PI is currently not known. In particular, the association between HC subfield volumes and control of PI in WM has not been examined previously. Here we investigate the associations between mean level and 5-year trajectories of gray matter subfield volumes and PI in WM across the adult life span (N = 157). Longitudinal analyses over 5-years across all participants revealed that reduced volume in the subiculum was related to impaired control of PI. Age-stratified analyses showed that this association was most pronounced in older adults. Furthermore, we found that in older adults the effect of age on PI was mediated by GM volume in the HC. The current results show that HC volume is associated with the ability to control PI in WM, and that these associations are modulated by age.

Place, publisher, year, edition, pages
Elsevier, 2023
National Category
Gerontology, specialising in Medical and Health Sciences Neurosciences
Identifiers
urn:nbn:se:umu:diva-216196 (URN)10.1016/j.ynirp.2023.100189 (DOI)2-s2.0-85175081750 (Scopus ID)
Funder
Swedish Research Council, 345-2003-3883Swedish Research Council, 315-2004-6977Swedish Research Council, 421-2013-1039
Available from: 2023-11-08 Created: 2023-11-08 Last updated: 2023-11-08Bibliographically approved
Nyberg, L., Andersson, M., Lundquist, A., Baaré, W. F. .., Bartrés-Faz, D., Bertram, L., . . . Walhovd, K. B. (2023). Individual differences in brain aging: heterogeneity in cortico-hippocampal but not caudate atrophy rates. Cerebral Cortex, 33(9), 5075-5081
Open this publication in new window or tab >>Individual differences in brain aging: heterogeneity in cortico-hippocampal but not caudate atrophy rates
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2023 (English)In: Cerebral Cortex, ISSN 1047-3211, E-ISSN 1460-2199, Vol. 33, no 9, p. 5075-5081Article in journal (Refereed) Published
Abstract [en]

It is well documented that some brain regions, such as association cortices, caudate, and hippocampus, are particularly prone to age-related atrophy, but it has been hypothesized that there are individual differences in atrophy profiles. Here, we document heterogeneity in regional-atrophy patterns using latent-profile analysis of 1,482 longitudinal magnetic resonance imaging observations. The results supported a 2-group solution reflecting differences in atrophy rates in cortical regions and hippocampus along with comparable caudate atrophy. The higher-atrophy group had the most marked atrophy in hippocampus and also lower episodic memory, and their normal caudate atrophy rate was accompanied by larger baseline volumes. Our findings support and refine models of heterogeneity in brain aging and suggest distinct mechanisms of atrophy in striatal versus hippocampal-cortical systems.

Place, publisher, year, edition, pages
Oxford University Press, 2023
Keywords
aging, individual differences, caudate, hippocampus, cortex
National Category
Neurosciences
Research subject
Medicine
Identifiers
urn:nbn:se:umu:diva-201287 (URN)10.1093/cercor/bhac400 (DOI)000863898100001 ()36197324 (PubMedID)2-s2.0-85159256770 (Scopus ID)
Funder
Knut and Alice Wallenberg FoundationEU, Horizon 2020, 732592
Available from: 2022-11-27 Created: 2022-11-27 Last updated: 2023-06-07Bibliographically approved
Nyberg, L., Andersson, M. & Lundquist, A. (2023). Longitudinal change-change associations of cognition with cortical thickness and surface area. Aging Brain, 3, Article ID 100070.
Open this publication in new window or tab >>Longitudinal change-change associations of cognition with cortical thickness and surface area
2023 (English)In: Aging Brain, E-ISSN 2589-9589, Vol. 3, article id 100070Article in journal (Refereed) Published
Abstract [en]

Age-related changes in cortical volumes are well established but relatively few studies probed its constituents, surface area (SA) and thickness (TH). Here we analyzed 10-year, 3-waves longitudinal data from a large sample of healthy individuals (baseline age = 55-80). The findings showed marked age-related changes of SA in frontal, temporal, and parietal association cortices, and Bivariate Latent Change Score models revealed significant SAassociations with changes in speed of processing in both the 5- and 10-year models. The corresponding results for TH revealed a late onset of thinning and significant associations with reduced cognition in the 10-year model only. Taken together, our findings suggest that cortical surface area shrinks and impacts information-processing capacity gradually in aging, whereas cortical thinning only manifests and impacts fluid cognition in advanced aging. 

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Cortex, Thickness, Surface area, Cognition, Speed
National Category
Neurosciences Neurology
Identifiers
urn:nbn:se:umu:diva-222727 (URN)10.1016/j.nbas.2023.100070 (DOI)001133947400001 ()37408792 (PubMedID)2-s2.0-85190996603 (Scopus ID)
Funder
Knut and Alice Wallenberg FoundationSwedish Research Council, 2018-05973
Available from: 2024-03-26 Created: 2024-03-26 Last updated: 2024-10-25Bibliographically approved
Nelson, A., Malmberg Gavelin, H., Andersson, M., Josefsson, M., Eskilsson, T., Slunga-Järvholm, L., . . . Boraxbekk, C.-J. (2023). Subjective cognitive complaints and its associations to response inhibition and neural activation in patients with stress-related exhaustion disorder. Stress, 26(1), Article ID 2188092.
Open this publication in new window or tab >>Subjective cognitive complaints and its associations to response inhibition and neural activation in patients with stress-related exhaustion disorder
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2023 (English)In: Stress, ISSN 1025-3890, E-ISSN 1607-8888, Vol. 26, no 1, article id 2188092Article in journal (Refereed) Published
Abstract [en]

Stress-related exhaustion is associated with cognitive deficits, measured subjectively using questionnaires targeting everyday slips and failures or more objectively as performance on cognitive tests. Yet, only weak associations between subjective and objective cognitive measures in this group has been presented, theorized to reflect recruitment of compensational resources during cognitive testing. This explorative study investigated how subjectively reported symptoms of cognitive functioning and burnout levels relate to performance as well as neural activation during a response inhibition task. To this end, 56 patients diagnosed with stress-related exhaustion disorder (ED; ICD-10 code F43.8A) completed functional magnetic resonance imaging (fMRI) using a Flanker paradigm. In order to investigate associations between neural activity and subjective cognitive complaints (SCCs) and burnout, respectively, scores on the Prospective and retrospective memory questionnaire (PRMQ) and the Shirom-Melamed burnout questionnaire (SMBQ) were added as covariates of interest to a general linear model at the whole-brain level. In agreement with previous research, the results showed that SCCs and burnout levels were largely unrelated to task performance. Moreover, we did not see any correlations between these self-report measures and altered neural activity in frontal brain regions. Instead, we observed an association between the PRMQ and increased neural activity in an occipitally situated cluster. We propose that this finding may reflect compensational processes at the level of basic visual attention which may go unnoticed in cognitive testing but are reflected in the experience of deficits in everyday cognitive functioning.

Place, publisher, year, edition, pages
Taylor & Francis, 2023
National Category
Neurosciences Public Health, Global Health, Social Medicine and Epidemiology Psychiatry
Identifiers
urn:nbn:se:umu:diva-205760 (URN)10.1080/10253890.2023.2188092 (DOI)000953639900001 ()36883330 (PubMedID)2-s2.0-85150665693 (Scopus ID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2009-0772Forte, Swedish Research Council for Health, Working Life and Welfare, 2020-01111)Region VästerbottenAFA InsuranceRiksbankens JubileumsfondThe Kempe Foundations
Available from: 2023-03-17 Created: 2023-03-17 Last updated: 2024-07-02Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-4743-6365

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