Publications by authors named "Anders M Fjell"

184 Publications

Education and Income Show Heterogeneous Relationships to Lifespan Brain and Cognitive Differences Across European and US Cohorts.

Cereb Cortex 2021 Aug 31. Epub 2021 Aug 31.

Center for Lifespan Psychology, Max Planck Institute for Human Development, Berlin 14195, Germany.

Higher socio-economic status (SES) has been proposed to have facilitating and protective effects on brain and cognition. We ask whether relationships between SES, brain volumes and cognitive ability differ across cohorts, by age and national origin. European and US cohorts covering the lifespan were studied (4-97 years, N = 500 000; 54 000 w/brain imaging). There was substantial heterogeneity across cohorts for all associations. Education was positively related to intracranial (ICV) and total gray matter (GM) volume. Income was related to ICV, but not GM. We did not observe reliable differences in associations as a function of age. SES was more strongly related to brain and cognition in US than European cohorts. Sample representativity varies, and this study cannot identify mechanisms underlying differences in associations across cohorts. Differences in neuroanatomical volumes partially explained SES-cognition relationships. SES was more strongly related to ICV than to GM, implying that SES-cognition relations in adulthood are less likely grounded in neuroprotective effects on GM volume in aging. The relatively stronger SES-ICV associations rather are compatible with SES-brain volume relationships being established early in life, as ICV stabilizes in childhood. The findings underscore that SES has no uniform association with, or impact on, brain and cognition.
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http://dx.doi.org/10.1093/cercor/bhab248DOI Listing
August 2021

Relationships between apparent cortical thickness and working memory across the lifespan - Effects of genetics and socioeconomic status.

Dev Cogn Neurosci 2021 Aug 8;51:100997. Epub 2021 Aug 8.

Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0317, Oslo, Norway; Department of Radiology and Nuclear Medicine, Oslo University Hospital, 0372, Oslo, Norway. Electronic address:

Working memory (WM) supports several higher-level cognitive abilities, yet we know less about factors associated with development and decline in WM compared to other cognitive processes. Here, we investigated lifespan changes in WM capacity and their structural brain correlates, using a longitudinal sample including 2358 magnetic resonance imaging (MRI) scans and WM scores from 1656 participants (4.4-86.4 years, mean follow-up interval 4.3 years). 8764 participants (9.0-10.9 years) with MRI, WM scores and genetic information from the Adolescent Brain Cognitive Development study were used for follow-up analyses. Results showed that both the information manipulation component and the storage component of WM improved during childhood and adolescence, but the age-decline could be fully explained by reductions in passive storage capacity alone. Greater WM function in development was related to apparent thinner cortex in both samples, also when general cognitive function was accounted for. The same WM-apparent thickness relationship was found for young adults. The WM-thickness relationships could not be explained by SNP-based co-heritability or by socioeconomic status. A larger sample with genetic information may be necessary to disentangle the true gene-environment effects. In conclusion, WM capacity changes greatly through life and has anatomically extended rather than function-specific structural cortical correlates.
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http://dx.doi.org/10.1016/j.dcn.2021.100997DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8371229PMC
August 2021

Reliability and sensitivity of two whole-brain segmentation approaches included in FreeSurfer - ASEG and SAMSEG.

Neuroimage 2021 08 1;237:118113. Epub 2021 May 1.

Center for Lifespan Changes in Brain and Cognition, University of Oslo, Pb. 1094, Blindern, Oslo 0317, Norway; Division of Radiology and Nuclear Medicine, Oslo University Hospital, Norway.

Accurate and reliable whole-brain segmentation is critical to longitudinal neuroimaging studies. We undertake a comparative analysis of two subcortical segmentation methods, Automatic Segmentation (ASEG) and Sequence Adaptive Multimodal Segmentation (SAMSEG), recently provided in the open-source neuroimaging package FreeSurfer 7.1, with regard to reliability, bias, sensitivity to detect longitudinal change, and diagnostic sensitivity to Alzheimer's disease. First, we assess intra- and inter-scanner reliability for eight bilateral subcortical structures: amygdala, caudate, hippocampus, lateral ventricles, nucleus accumbens, pallidum, putamen and thalamus. For intra-scanner analysis we use a large sample of participants (n = 1629) distributed across the lifespan (age range = 4-93 years) and acquired on a 1.5T Siemens Avanto (n = 774) and a 3T Siemens Skyra (n = 855) scanners. For inter-scanner analysis we use a sample of 24 participants scanned on the day with three models of Siemens scanners: 1.5T Avanto, 3T Skyra and 3T Prisma. Second, we test how each method detects volumetric age change using longitudinal follow up scans (n = 491 for Avanto and n = 245 for Skyra; interscan interval = 1-10 years). Finally, we test sensitivity to clinically relevant change. We compare annual rate of hippocampal atrophy in cognitively normal older adults (n = 20), patients with mild cognitive impairment (n = 20) and Alzheimer's disease (n = 20). We find that both ASEG and SAMSEG are reliable and lead to the detection of within-person longitudinal change, although with notable differences between age-trajectories for most structures, including hippocampus and amygdala. In summary, SAMSEG yields significantly lower differences between repeated measures for intra- and inter-scanner analysis without compromising sensitivity to changes and demonstrating ability to detect clinically relevant longitudinal changes.
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http://dx.doi.org/10.1016/j.neuroimage.2021.118113DOI Listing
August 2021

Self-Reported Sleep Relates to Microstructural Hippocampal Decline in β-Amyloid Positive Adults Beyond Genetic Risk.

Sleep 2021 Apr 27. Epub 2021 Apr 27.

Research Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0317 Oslo, Norway.

Study Objectives: A critical role linking sleep with memory decay and β-amyloid (Aβ) accumulation, two markers of Alzheimer's disease (AD) pathology, may be played by hippocampal integrity. We tested the hypotheses that worse self-reported sleep relates to decline in memory and intra-hippocampal microstructure, including in the presence of Aβ.

Methods: Two-hundred and forty-three cognitively healthy participants, aged 19-81 years, completed the Pittsburgh Sleep Quality Index once, and 2 diffusion tensor imaging sessions, on average 3 years apart, allowing measures of decline in intra-hippocampal microstructure as indexed by increased mean diffusivity. We measured memory decay at each imaging session using verbal delayed recall. One session of positron emission tomography, in 108 participants above 44 years of age, yielded 23 Aβ positive. Genotyping enabled control for APOE ε4 status, and polygenic scores for sleep and AD, respectively.

Results: Worse global sleep quality and sleep efficiency related to more rapid reduction of hippocampal microstructure over time. Focusing on efficiency (the percentage of time in bed at night spent asleep), the relation was stronger in presence of Aβ accumulation, and hippocampal integrity decline mediated the relation with memory decay. The results were not explained by genetic risk for sleep efficiency or AD.

Conclusions: Worse sleep efficiency related to decline in hippocampal microstructure, especially in the presence of Aβ accumulation, and Aβ might link poor sleep and memory decay. As genetic risk did not account for the associations, poor sleep efficiency might constitute a risk marker for AD, although the driving causal mechanisms remain unknown.
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http://dx.doi.org/10.1093/sleep/zsab110DOI Listing
April 2021

Educational attainment does not influence brain aging.

Proc Natl Acad Sci U S A 2021 May;118(18)

Center for Lifespan Changes in Brain and Cognition, University of Oslo, 0317 Oslo, Norway;

Education has been related to various advantageous lifetime outcomes. Here, using longitudinal structural MRI data (4,422 observations), we tested the influential hypothesis that higher education translates into slower rates of brain aging. Cross-sectionally, education was modestly associated with regional cortical volume. However, despite marked mean atrophy in the cortex and hippocampus, education did not influence rates of change. The results were replicated across two independent samples. Our findings challenge the view that higher education slows brain aging.
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http://dx.doi.org/10.1073/pnas.2101644118DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8106299PMC
May 2021

Development of attention networks from childhood to young adulthood: A study of performance, intraindividual variability and cortical thickness.

Cortex 2021 05 13;138:138-151. Epub 2021 Feb 13.

PROMENTA Research Center, Department of Psychology, University of Oslo, Oslo, Norway; NORMENT, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Psychiatric Research, Diakonhjemmet Hospital, Oslo, Norway.

Human cognitive development is manifold, with different functions developing at different speeds at different ages. Attention is an important domain of this cognitive development, and involves distinct developmental trajectories for separate functions, including conflict processing, selection of sensory input and alertness. In children, several studies using the Attention Network Test (ANT) have investigated the development of three attentional networks that carry out the functions of executive control, orienting and alerting. There is, however, a lack of studies on the development of these attentional components across adolescence, limiting our understanding of their protracted development. To fill this knowledge gap, we performed a mixed cross-sectional and longitudinal study using mixed methods to examine the development of the attentional components and their intraindividual variability from late childhood to young adulthood (n = 287, n observations = 408, age range = 8.5-26.7 years, mean follow up interval = 4.4 years). The results indicated that executive control stabilized during late adolescence, while orienting and alerting continued to develop into young adulthood. In addition, a continuous development into young adulthood was observed for the intraindividual variability measures of orienting and alerting. In a subsample with available magnetic resonance imaging (MRI) data (n = 169, n observations = 281), higher alerting scores were associated with thicker cortices within a right prefrontal cortical region and greater age-related cortical thinning in left rolandic operculum, while higher orienting scores were associated with greater age-related cortical thinning in frontal and parietal regions. Finally, increased consistency of orienting performance was associated with thinner cortex in prefrontal regions and reduced age-related thinning in frontal regions.
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http://dx.doi.org/10.1016/j.cortex.2021.01.018DOI Listing
May 2021

Electrophysiological and behavioral indices of cognitive conflict processing across adolescence.

Dev Cogn Neurosci 2021 04 27;48:100929. Epub 2021 Jan 27.

Multimodal Imaging and Cognitive Control Lab, Department of Psychology, University of Oslo, Oslo, Norway; Cognitive and Translational Neuroscience Cluster, Department of Psychology, University of Oslo, Oslo, Norway.

Cognitive control enables goal-oriented adaptation to a fast-changing environment and has a protracted development spanning into young adulthood. The neurocognitive processes underlying this development are poorly understood. In a cross-sectional sample of participants 8-19 years old (n = 108), we used blind source separation of EEG data recorded in a Flanker task to derive electrophysiological measures of attention and conflict processing, including a N2-like frontal negative component and a P3-like parietal positive component. Outside the recording session, we examined multiple behavioral measures of interference control derived from the Flanker, Stroop, and Anti-saccade tasks. We found a positive association between age and P3 amplitude, but no relationship between age and N2 amplitude. A stronger N2 was age-independently related to better performance on Stroop and Anti-saccade measures of interference control. A Gratton effect was found on the Flanker task, with slower reaction times on current congruent and better accuracy on current incongruent trials when preceded by incongruent as opposed to congruent trials. The Gratton effect on accuracy was positively associated with age. Together, the findings suggest a multifaceted developmental pattern of the neurocognitive processes involved in conflict processing across adolescence, with a more protracted development of the P3 compared to the N2.
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http://dx.doi.org/10.1016/j.dcn.2021.100929DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7868601PMC
April 2021

Cognitive reappraisal and expressive suppression relate differentially to longitudinal structural brain development across adolescence.

Cortex 2021 03 12;136:109-123. Epub 2021 Jan 12.

PROMENTA Research Center, Department of Psychology, University of Oslo, Oslo, Norway; Department of Psychiatric Research, Diakonhjemmet Hospital, Oslo, Norway; Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Electronic address:

Emotional disorders commonly emerge in adolescence, a period characterized by changes in emotion-related processes. Thus, the ability to regulate emotions is crucial for well-being and adaptive social functioning during this period. Concurrently, the brain undergoes large structural and functional changes. We investigated relations between tendencies to use two emotion regulation strategies, cognitive reappraisal and expressive suppression, and structural development of the cerebral cortex and subcortical structures (specifically amygdala and nucleus accumbens given these structures are frequently associated with emotion regulation). A total of 112 participants (59 females) aged 8-26 were followed for up to 3 times over a 7-year period, providing 272 observations. Participants completed the Emotion Regulation Questionnaire (ERQ), yielding a measure of tendencies to use cognitive reappraisal and expressive suppression at the final time point. Linear mixed model analyses were performed to account for the longitudinal nature of the data. Contrary to expectations, volumetric growth of the amygdala and nucleus accumbens was not associated with either emotion regulation strategy. However, frequent use of expressive suppression was linked to greater regionally-specific apparent cortical thinning in both sexes, while tendency to use cognitive reappraisal was associated with greater regionally-specific apparent thinning in females and less thinning in males. Although cognitive reappraisal is traditionally associated with cognitive control regions of the brain, our results suggest it is also associated with regions involved in social cognition and semantics. The continued changes in cortical morphology and their associations with habitual use of different emotion regulation strategies indicate continued plasticity during this period, and represent an opportunity for interventions targeting emotion regulation for adolescents at risk.
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http://dx.doi.org/10.1016/j.cortex.2020.11.022DOI Listing
March 2021

Asymmetric thinning of the cerebral cortex across the adult lifespan is accelerated in Alzheimer's disease.

Nat Commun 2021 02 1;12(1):721. Epub 2021 Feb 1.

Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, Oslo, Norway.

Aging and Alzheimer's disease (AD) are associated with progressive brain disorganization. Although structural asymmetry is an organizing feature of the cerebral cortex it is unknown whether continuous age- and AD-related cortical degradation alters cortical asymmetry. Here, in multiple longitudinal adult lifespan cohorts we show that higher-order cortical regions exhibiting pronounced asymmetry at age ~20 also show progressive asymmetry-loss across the adult lifespan. Hence, accelerated thinning of the (previously) thicker homotopic hemisphere is a feature of aging. This organizational principle showed high consistency across cohorts in the Lifebrain consortium, and both the topological patterns and temporal dynamics of asymmetry-loss were markedly similar across replicating samples. Asymmetry-change was further accelerated in AD. Results suggest a system-wide dedifferentiation of the adaptive asymmetric organization of heteromodal cortex in aging and AD.
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http://dx.doi.org/10.1038/s41467-021-21057-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7851164PMC
February 2021

Cellular correlates of cortical thinning throughout the lifespan.

Sci Rep 2020 12 11;10(1):21803. Epub 2020 Dec 11.

Centre for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, Pb. 1094 Blindern, 0317, Oslo, Norway.

Cortical thinning occurs throughout the entire life and extends to late-life neurodegeneration, yet the neurobiological substrates are poorly understood. Here, we used a virtual-histology technique and gene expression data from the Allen Human Brain Atlas to compare the regional profiles of longitudinal cortical thinning through life (4004 magnetic resonance images [MRIs]) with those of gene expression for several neuronal and non-neuronal cell types. The results were replicated in three independent datasets. We found that inter-regional profiles of cortical thinning related to expression profiles for marker genes of CA1 pyramidal cells, astrocytes and, microglia during development and in aging. During the two stages of life, the relationships went in opposite directions: greater gene expression related to less thinning in development and vice versa in aging. The association between cortical thinning and cell-specific gene expression was also present in mild cognitive impairment and Alzheimer's Disease. These findings suggest a role of astrocytes and microglia in promoting and supporting neuronal growth and dendritic structures through life that affects cortical thickness during development, aging, and neurodegeneration. Overall, the findings contribute to our understanding of the neurobiology underlying variations in MRI-derived estimates of cortical thinning through life and late-life disease.
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http://dx.doi.org/10.1038/s41598-020-78471-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7732849PMC
December 2020

Within-session verbal learning slope is predictive of lifespan delayed recall, hippocampal volume, and memory training benefit, and is heritable.

Sci Rep 2020 12 3;10(1):21158. Epub 2020 Dec 3.

Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, POB 1094, 0317, Oslo, Norway.

Memory performance results from plasticity, the ability to change with experience. We show that benefit from practice over a few trials, learning slope, is predictive of long-term recall and hippocampal volume across a broad age range and a long period of time, relates to memory training benefit, and is heritable. First, in a healthy lifespan sample (n = 1825, age 4-93 years), comprising 3483 occasions of combined magnetic resonance imaging (MRI) scans and memory tests over a period of up to 11 years, learning slope across 5 trials was uniquely related to performance on a delayed free recall test, as well as hippocampal volume, independent from first trial memory or total memory performance across the five learning trials. Second, learning slope was predictive of benefit from memory training across ten weeks in an experimental subsample of adults (n = 155). Finally, in an independent sample of male twins (n = 1240, age 51-50 years), learning slope showed significant heritability. Within-session learning slope may be a useful marker beyond performance per se, being heritable and having unique predictive value for long-term memory function, hippocampal volume and training benefit across the human lifespan.
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http://dx.doi.org/10.1038/s41598-020-78225-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7713377PMC
December 2020

The Functional Foundations of Episodic Memory Remain Stable Throughout the Lifespan.

Cereb Cortex 2021 03;31(4):2098-2110

Department of Psychology, Centre for Lifespan Changes in Brain and Cognition, University of Oslo, Oslo 0317, Norway.

It has been suggested that specific forms of cognition in older age rely largely on late-life specific mechanisms. Here instead, we tested using task-fMRI (n = 540, age 6-82 years) whether the functional foundations of successful episodic memory encoding adhere to a principle of lifespan continuity, shaped by developmental, structural, and evolutionary influences. We clustered regions of the cerebral cortex according to the shape of the lifespan trajectory of memory activity in each region so that regions showing the same pattern were clustered together. The results revealed that lifespan trajectories of memory encoding function showed a continuity through life but no evidence of age-specific mechanisms such as compensatory patterns. Encoding activity was related to general cognitive abilities and variations of grey matter as captured by a multi-modal independent component analysis, variables reflecting core aspects of cognitive and structural change throughout the lifespan. Furthermore, memory encoding activity aligned to fundamental aspects of brain organization, such as large-scale connectivity and evolutionary cortical expansion gradients. Altogether, we provide novel support for a perspective on memory aging in which maintenance and decay of episodic memory in older age needs to be understood from a comprehensive life-long perspective rather than as a late-life phenomenon only.
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http://dx.doi.org/10.1093/cercor/bhaa348DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7945016PMC
March 2021

A recipe for accurate estimation of lifespan brain trajectories, distinguishing longitudinal and cohort effects.

Neuroimage 2021 02 26;226:117596. Epub 2020 Nov 26.

Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, Norway; Department of Radiology and Nuclear Medicine, Oslo University Hospital, Norway.

We address the problem of estimating how different parts of the brain develop and change throughout the lifespan, and how these trajectories are affected by genetic and environmental factors. Estimation of these lifespan trajectories is statistically challenging, since their shapes are typically highly nonlinear, and although true change can only be quantified by longitudinal examinations, as follow-up intervals in neuroimaging studies typically cover less than 10% of the lifespan, use of cross-sectional information is necessary. Linear mixed models (LMMs) and structural equation models (SEMs) commonly used in longitudinal analysis rely on assumptions which are typically not met with lifespan data, in particular when the data consist of observations combined from multiple studies. While LMMs require a priori specification of a polynomial functional form, SEMs do not easily handle data with unstructured time intervals between measurements. Generalized additive mixed models (GAMMs) offer an attractive alternative, and in this paper we propose various ways of formulating GAMMs for estimation of lifespan trajectories of 12 brain regions, using a large longitudinal dataset and realistic simulation experiments. We show that GAMMs are able to more accurately fit lifespan trajectories, distinguish longitudinal and cross-sectional effects, and estimate effects of genetic and environmental exposures. Finally, we discuss and contrast questions related to lifespan research which strictly require repeated measures data and questions which can be answered with a single measurement per participant, and in the latter case, which simplifying assumptions that need to be made. The examples are accompanied with R code, providing a tutorial for researchers interested in using GAMMs.
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http://dx.doi.org/10.1016/j.neuroimage.2020.117596DOI Listing
February 2021

Poor Self-Reported Sleep is Related to Regional Cortical Thinning in Aging but not Memory Decline-Results From the Lifebrain Consortium.

Cereb Cortex 2021 03;31(4):1953-1969

Center for Lifespan Changes in Brain and Cognition, University of Oslo, 0315 Oslo, Norway.

We examined whether sleep quality and quantity are associated with cortical and memory changes in cognitively healthy participants across the adult lifespan. Associations between self-reported sleep parameters (Pittsburgh Sleep Quality Index, PSQI) and longitudinal cortical change were tested using five samples from the Lifebrain consortium (n = 2205, 4363 MRIs, 18-92 years). In additional analyses, we tested coherence with cell-specific gene expression maps from the Allen Human Brain Atlas, and relations to changes in memory performance. "PSQI # 1 Subjective sleep quality" and "PSQI #5 Sleep disturbances" were related to thinning of the right lateral temporal cortex, with lower quality and more disturbances being associated with faster thinning. The association with "PSQI #5 Sleep disturbances" emerged after 60 years, especially in regions with high expression of genes related to oligodendrocytes and S1 pyramidal neurons. None of the sleep scales were related to a longitudinal change in episodic memory function, suggesting that sleep-related cortical changes were independent of cognitive decline. The relationship to cortical brain change suggests that self-reported sleep parameters are relevant in lifespan studies, but small effect sizes indicate that self-reported sleep is not a good biomarker of general cortical degeneration in healthy older adults.
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http://dx.doi.org/10.1093/cercor/bhaa332DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7945023PMC
March 2021

Genetic risk for Alzheimer disease predicts hippocampal volume through the human lifespan.

Neurol Genet 2020 Oct 8;6(5):e506. Epub 2020 Sep 8.

Center for Lifespan Changes in Brain and Cognition (K.B.W., A.M.F., Ø.S., A.M.M., C.S.R., A.-V.I., L.B., Y.W.), Department of Psychology, University of Oslo; Division of Radiology and Nuclear Medicine (K.B.W., A.M.F.), Oslo University Hospital, Rikshospitalet; Oslo Delirium Research Group (A.-V.I., L.O.W.), Department of Geriatric Medicine, and Institute of Basic Medical Sciences (A.-V.I., L.O.W.), University of Oslo, Norway; Institute of Clinical Molecular Biology (A.F.), Christian-Albrechts-University of Kiel; and Lübeck Interdisciplinary Platform for Genome Analytics (V.D., F.K., L.B.), Institutes of Neurogenetics and Cardiogenetics, University of Lübeck, Germany.

Objective: To test the hypothesis that genetic risk for Alzheimer disease (AD) may represent a stable influence on the brain from early in life, rather than being primarily age dependent, we investigated in a lifespan sample of 1,181 persons with a total of 2,690 brain scans, whether higher polygenic risk score (PGS) for AD and presence of ε4 was associated with lower hippocampal volumes to begin with, as an offset effect, or possibly faster decline in older age.

Methods: Using general additive mixed models, we assessed the relations of PGS for AD, including variants in with hippocampal volume and its change in a cognitively healthy longitudinal lifespan sample (age range: 4-95 years, mean visit age 39.7 years, SD 26.9 years), followed for up to 11 years.

Results: AD-PGS and ε4 in isolation showed a significant negative effect on hippocampal volume. The effect of a 1 sample SD increase in AD-PGS on hippocampal volume was estimated to -36.4 mm (confidence interval [CI]: -71.8, -1.04) and the effect of carrying ε4 allele(s) -107.0 mm (CI: -182.0, -31.5). Offset effects of AD-PGS and ε4 were present in hippocampal development, and interactions between age and genetic risk on volume change were not consistently observed.

Conclusions: Endophenotypic manifestation of polygenic risk for AD may be seen across the lifespan in cognitively healthy persons, not being confined to clinical populations or older age. This emphasizes that a broader population and age range may be relevant targets for attempts to prevent AD.
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http://dx.doi.org/10.1212/NXG.0000000000000506DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7577559PMC
October 2020

Amyloid-PET and F-FDG-PET in the diagnostic investigation of Alzheimer's disease and other dementias.

Lancet Neurol 2020 11;19(11):951-962

Department of Neurodegenerative Disease, Institute of Neurology, University College London, London, UK; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; UK Dementia Research Institute at University College London, London, UK.

Various biomarkers are available to support the diagnosis of neurodegenerative diseases in clinical and research settings. Among the molecular imaging biomarkers, amyloid-PET, which assesses brain amyloid deposition, and F-fluorodeoxyglucose (F-FDG) PET, which assesses glucose metabolism, provide valuable and complementary information. However, uncertainty remains regarding the optimal timepoint, combination, and an order in which these PET biomarkers should be used in diagnostic evaluations because conclusive evidence is missing. Following an expert panel discussion, we reached an agreement on the specific use of the individual biomarkers, based on available evidence and clinical expertise. We propose a diagnostic algorithm with optimal timepoints for these PET biomarkers, also taking into account evidence from other biomarkers, for early and differential diagnosis of neurodegenerative diseases that can lead to dementia. We propose three main diagnostic pathways with distinct biomarker sequences, in which amyloid-PET and F-FDG-PET are placed at different positions in the order of diagnostic evaluations, depending on clinical presentation. We hope that this algorithm can support diagnostic decision making in specialist clinical settings with access to these biomarkers and might stimulate further research towards optimal diagnostic strategies.
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http://dx.doi.org/10.1016/S1474-4422(20)30314-8DOI Listing
November 2020

Longitudinal association between hippocampus atrophy and episodic-memory decline in non-demented ε4 carriers.

Alzheimers Dement (Amst) 2020 28;12(1):e12110. Epub 2020 Sep 28.

Department of Integrative Medical Biology Umeå University Umeå Sweden.

Introduction: The apolipoprotein E () ε4 allele is the main genetic risk factor for Alzheimer's disease (AD), accelerated cognitive aging, and hippocampal atrophy, but its influence on the association between hippocampus atrophy and episodic-memory decline in non-demented individuals remains unclear.

Methods: We analyzed longitudinal (two to six observations) magnetic resonance imaging (MRI)-derived hippocampal volumes and episodic memory from 748 individuals (55 to 90 years at baseline, 50% female) from the European consortium.

Results: The change-change association for hippocampal volume and memory was significant only in ε4 carriers (N = 173, r = 0.21, = .007; non-carriers: N = 467, r = 0.073, = .117). The linear relationship was significantly steeper for the carriers [t(629) = 2.4, = .013]. A similar trend toward a stronger change-change relation for carriers was seen in a subsample with more than two assessments.

Discussion: These findings provide evidence for a difference in hippocampus-memory association between ε4 carriers and non-carriers, thus highlighting how genetic factors modulate the translation of the AD-related pathophysiological cascade into cognitive deficits.
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http://dx.doi.org/10.1002/dad2.12110DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521596PMC
September 2020

Comparative morphology of the corpus callosum across the adult lifespan in chimpanzees (Pan troglodytes) and humans.

J Comp Neurol 2021 05 26;529(7):1584-1596. Epub 2020 Sep 26.

Department of Comparative Medicine, Michael E. Keeling Center for Comparative Medicine and Research, UT MD Anderson Cancer Center, Bastrop, Texas, USA.

The human corpus callosum exhibits substantial atrophy in old age, which is stronger than what would be predicted from parallel changes in overall brain anatomy. To date, however, it has not been conclusively established whether this accentuated decline represents a common feature of brain aging across species, or whether it is a specific characteristic of the aging human brain. In the present cross-sectional study, we address this question by comparing age-related difference in corpus callosum morphology of chimpanzees and humans. For this purpose, we measured total midsagittal area and regional thickness of the corpus callosum from T1-weighted MRI data from 213 chimpanzees, aged between 9 and 54 years. The results were compared with data drawn from a large-scale human sample which was age-range matched using two strategies: (a) matching by chronological age (human sample size: n = 562), or (b) matching by accounting for differences in longevity and various maturational events between the species (i.e., adjusted human age range: 13.6 to 80.9 years; n = 664). Using generalized additive modeling to fit and compare aging trajectories, we found significant differences between the two species. The chimpanzee aging trajectory compared with the human trajectory was characterized by a slower increase from adolescence to middle adulthood, and by a lack of substantial decline from middle to old adulthood, which, however, was present in humans. Thus, the accentuated decline of the corpus callosum found in aging humans is not a universal characteristic of the aging brain, and appears to be human-specific.
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http://dx.doi.org/10.1002/cne.25039DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7987726PMC
May 2021

Level of body fat relates to memory decline and interacts with age in its association with hippocampal and subcortical atrophy.

Neurobiol Aging 2020 07 14;91:112-124. Epub 2019 Oct 14.

Department of Psychology, Center for Lifespan Changes in Brain and Cognition, University of Oslo, Oslo, Norway; Department of radiology and nuclear medicine, Oslo University Hospital, Oslo, Norway.

Higher levels of body fat have shown adverse effects on multiple aspects of health, including cognitive and neuroanatomical changes. We tested the relationships of body fat levels and cholesterol to longitudinal age trajectories of subcortical gray matter volume (SCV), hippocampal volume (HCV), and episodic memory. Body fat was indexed by a concerted factor of BMI, visceral adipose tissue, percentage body fat, and total fat mass and was included in the analyses as a cross-sectional measure. We hypothesized that higher level of body fat would be related to steeper age trajectories of SCV, HCV, and memory. The sample consisted of 581 participants (20-83 years) with 942 magnetic resonance imaging and 945 memory examinations. Using generalized additive mixed models, a negative effect of body fat was found on SCV, HCV, and memory. Age and body fat interacted in their association with brain volume change. The results suggest that among cognitively healthy adults, there is a negative effect of higher body fat on SCV, HCV, and memory decline, an effect that increased with age for the neuroanatomical volumes.
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http://dx.doi.org/10.1016/j.neurobiolaging.2019.10.005DOI Listing
July 2020

Self-reported Sleep Problems Related to Amyloid Deposition in Cortical Regions with High HOMER1 Gene Expression.

Cereb Cortex 2020 04;30(4):2144-2156

Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, Oslo 0317, Norway.

Sleep problems are related to the elevated levels of the Alzheimer's disease (AD) biomarker β-amyloid (Aβ). Hypotheses about the causes of this relationship can be generated from molecular markers of sleep problems identified in rodents. A major marker of sleep deprivation is Homer1a, a neural protein coded by the HOMER1 gene, which has also been implicated in brain Aβ accumulation. Here, we tested whether the relationship between cortical Aβ accumulation and self-reported sleep quality, as well as changes in sleep quality over 3 years, was stronger in cortical regions with high HOMER1 mRNA expression levels. In a sample of 154 cognitively healthy older adults, Aβ correlated with poorer sleep quality cross-sectionally and longitudinally (n = 62), but more strongly in the younger than in older individuals. Effects were mainly found in regions with high expression of HOMER1. The anatomical distribution of the sleep-Aβ relationship followed closely the Aβ accumulation pattern in 69 patients with mild cognitive impairment or AD. Thus, the results indicate that the relationship between sleep problems and Aβ accumulation may involve Homer1 activity in the cortical regions, where harbor Aβ deposits in AD. The findings may advance our understanding of the relationship between sleep problems and AD risk.
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http://dx.doi.org/10.1093/cercor/bhz228DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7174994PMC
April 2020

Risk- and protective factors for memory plasticity in aging.

Neuropsychol Dev Cogn B Aging Neuropsychol Cogn 2021 03 25;28(2):201-217. Epub 2020 Feb 25.

Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo , Oslo, Norway.

Risk and protective factors for cognitive function in aging may affect how much individuals benefit from their environment or life experiences by preserving or improving cognitive abilities. We investigated the relations between such factors and outcome from episodic-memory training in 136 healthy young and older adults. Tested risk factors included carrying the ɛ4 variant of the apolipoprotein E allele (APOE), age, body mass index, blood pressure, and cholesterol. Protective factors included higher levels of education, intelligence quotient (IQ), physical activity, fatty acids, and vitamin D. Average increases in memory performance were seen after training, with ample variation between individuals. Being young, female, and having higher IQ were positive predictors of memory improvement. No other relationships were observed. Similar benefit was observed across APOE allelic variation. This indicates that beyond IQ, age, and sex, known risk -and protective factors of cognitive function in aging were not significantly related to memory plasticity.
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http://dx.doi.org/10.1080/13825585.2020.1727834DOI Listing
March 2021

Anterior and posterior hippocampus macro- and microstructure across the lifespan in relation to memory-A longitudinal study.

Hippocampus 2020 07 21;30(7):678-692. Epub 2020 Jan 21.

Center for Lifespan Changes in Brain and Cognition, University of Oslo, Norway.

There is evidence for a hippocampal long axis anterior-posterior (AP) differentiation in memory processing, which may have implications for the changes in episodic memory performance seen across development and aging. The hippocampus shows substantial structural changes with age, but the lifespan trajectories of hippocampal sub-regions along the AP axis are not established. The aim of the present study was to test whether the micro- and macro-structural age-trajectories of the anterior (aHC) and posterior (pHC) hippocampus are different. In a single-center longitudinal study, 1,790 cognitively healthy participants, 4.1-93.4 years of age, underwent a total of 3,367 MRI examinations and 3,033 memory tests sessions over 1-6 time points, spanning an interval up to 11.1 years. T1-weighted scans were used to estimate the volume of aHC and pHC (macrostructure), and diffusion tensor imaging to measure mean diffusion (MD, microstructure) within each region. We found that the macro- and microstructural lifespan-trajectories of aHC and pHC were clearly distinguishable, with partly common and partly unique variance shared with age. aHC showed a protracted period of microstructural development, while pHC microstructural development as indexed by MD was more or less completed in early childhood. In contrast, pHC showed larger unique aging-related changes. An aHC-pHC difference was also observed for volume, with pHC changing relatively more with higher age. All regions showed age-dependent relationships with episodic memory. aHC micro- and macrostructure was significantly related to verbal memory independently of age, but the relationships were still strongest among the older participants. We suggest that memory processes supported by each sub-region improve or decline in concert with volumetric and microstructural changes in the same age-period. Future research should disentangle the lifespan relationship between changes in these structural properties and different memory processes, encoding versus retrieval in particular, as well as other cognitive functions depending on the hippocampal long-axis specialization.
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http://dx.doi.org/10.1002/hipo.23189DOI Listing
July 2020

CSF sTREM2 and Tau Work Together in Predicting Increased Temporal Lobe Atrophy in Older Adults.

Cereb Cortex 2020 04;30(4):2295-2306

Department of Psychology, Center for Lifespan Changes in Brain and Cognition, University of Oslo, 0373 Oslo, Norway.

Neuroinflammation may be a key factor in brain atrophy in aging and age-related neurodegenerative disease. The objective of this study was to test the association between microglial expression of soluble Triggering Receptor Expressed on Myeloid Cells 2 (sTREM2), as a measure of neuroinflammation, and brain atrophy in cognitively unimpaired older adults. Brain magnetic resonance imagings (MRIs) and cerebrospinal fluid (CSF) sTREM2, total tau (t-tau), phosphorylated181 tau (p-tau), and Aβ42 were analyzed in 115 cognitively unimpaired older adults, classified according to the A/T/(N)-framework. MRIs were repeated after 2 (n = 95) and 4 (n = 62) years. High baseline sTREM2 was associated with accelerated cortical thinning in the temporal cortex of the left hemisphere, as well as bilateral hippocampal atrophy, independently of age, Aβ42, and tau. sTREM2-related atrophy only marginally increased with biomarker positivity across the AD continuum (A-T- #x2292; A+T- #x2292; A+T+) but was significantly stronger in participants with a high level of p-tau (T+). sTREM2-related cortical thinning correlated significantly with areas of high microglial-specific gene expression in the Allen Human Brain Atlas. In conclusion, increased CSF sTREM2 was associated with accelerated cortical and hippocampal atrophy in cognitively unimpaired older participants, particularly in individuals with tau pathology. This suggests a link between neuroinflammation, neurodegeneration, and amyloid-independent tauopathy.
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http://dx.doi.org/10.1093/cercor/bhz240DOI Listing
April 2020

Prosocial behavior relates to the rate and timing of cortical thinning from adolescence to young adulthood.

Dev Cogn Neurosci 2019 12 6;40:100734. Epub 2019 Nov 6.

PROMENTA Research Center, Department of Psychology, University of Oslo, Department of Psychiatry, Diakonhjemmet Hospital, NORMENT, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Electronic address:

Prosocial behavior, or voluntary actions that intentionally benefit others, relate to desirable developmental outcomes such as peer acceptance, while lack of prosocial behavior has been associated with several neurodevelopmental disorders. Mapping the biological foundations of prosociality may thus aid our understanding of both normal and abnormal development, yet how prosociality relates to cortical development is largely unknown. Here, relations between prosociality, as measured by the Strengths and Difficulties Questionnaire (self-report), and changes in thickness across the cortical mantle were examined using mixed-effects models. The sample consisted of 169 healthy individuals (92 females) aged 12-26 with repeated MRI from up to 3 time points, at approximately 3-year intervals (301 scans). In regions associated with social cognition and behavioral control, higher prosociality was associated with greater cortical thinning during early-to-middle adolescence, followed by attenuation of this process during the transition to young adulthood. Comparatively, lower prosociality was related to initially slower thinning, followed by comparatively protracted thinning into the mid-twenties. This study showed that prosocial behavior is associated with regional development of cortical thickness in adolescence and young adulthood. The results suggest that the rate of thinning in these regions, as well as its timing, may be factors related to prosocial behavior.
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http://dx.doi.org/10.1016/j.dcn.2019.100734DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974908PMC
December 2019

Self-reported sleep relates to hippocampal atrophy across the adult lifespan: results from the Lifebrain consortium.

Sleep 2020 05;43(5)

Center for Lifespan Changes in Brain and Cognition, University of Oslo, Norway.

Objectives: Poor sleep is associated with multiple age-related neurodegenerative and neuropsychiatric conditions. The hippocampus plays a special role in sleep and sleep-dependent cognition, and accelerated hippocampal atrophy is typically seen with higher age. Hence, it is critical to establish how the relationship between sleep and hippocampal volume loss unfolds across the adult lifespan.

Methods: Self-reported sleep measures and MRI-derived hippocampal volumes were obtained from 3105 cognitively normal participants (18-90 years) from major European brain studies in the Lifebrain consortium. Hippocampal volume change was estimated from 5116 MRIs from 1299 participants for whom longitudinal MRIs were available, followed up to 11 years with a mean interval of 3.3 years. Cross-sectional analyses were repeated in a sample of 21,390 participants from the UK Biobank.

Results: No cross-sectional sleep-hippocampal volume relationships were found. However, worse sleep quality, efficiency, problems, and daytime tiredness were related to greater hippocampal volume loss over time, with high scorers showing 0.22% greater annual loss than low scorers. The relationship between sleep and hippocampal atrophy did not vary across age. Simulations showed that the observed longitudinal effects were too small to be detected as age-interactions in the cross-sectional analyses.

Conclusions: Worse self-reported sleep is associated with higher rates of hippocampal volume decline across the adult lifespan. This suggests that sleep is relevant to understand individual differences in hippocampal atrophy, but limited effect sizes call for cautious interpretation.
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http://dx.doi.org/10.1093/sleep/zsz280DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7215271PMC
May 2020

Are People Ready for Personalized Brain Health? Perspectives of Research Participants in the Lifebrain Consortium.

Gerontologist 2020 08;60(6):1050-1059

Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, Norway.

Background And Objectives: A healthy brain is central to physical and mental well-being. In this multi-site, qualitative study, we investigated views and attitudes of adult participants in brain research studies on the brain and personalized brain health as well as interest in maintaining a healthy brain.

Design And Methods: We conducted individual interviews with 44 adult participants in brain research cohorts of the Lifebrain consortium in Spain, Norway, Germany, and the United Kingdom. The interviews were audio recorded, transcribed, and coded using a cross-country codebook. The interview data were analyzed using qualitative content analysis.

Results: Most participants did not focus on their own brain health and expressed uncertainty regarding how to maintain it. Those actively focusing on brain health often picked one specific strategy like diet or memory training. The participants were interested in taking brain health tests to learn about their individual risk of developing brain diseases, and were willing to take measures to maintain their brain health if personalized follow-up was provided and the measures had proven impact. The participants were interested in more information on brain health. No differences in responses were identified between age groups, sex, or countries.

Discussion And Implications: Concise, practical, personalized, and evidence-based information about the brain may promote brain health. Based on our findings, we have launched an ongoing global brain health survey to acquire more extensive, quantitative, and representative data on public perception of personalized brain health.
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http://dx.doi.org/10.1093/geront/gnz155DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427479PMC
August 2020

Volumetric and microstructural regional changes of the hippocampus underlying development of recall performance after extended retention intervals.

Dev Cogn Neurosci 2019 12 22;40:100723. Epub 2019 Oct 22.

Center for Lifespan Changes in Brain and Cognition, University of Oslo, Norway; Department of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway.

Performance on recall tests improves through childhood and adolescence, in part due to structural maturation of the medial temporal cortex. Although partly different processes support successful recall over shorter vs. longer intervals, recall is usually tested after less than an hour. The aim of the present study was to test whether there are unique developmental changes in recall performance using extended retention intervals, and whether these are related to structural maturation of sub-regions of the hippocampus. 650 children and adolescents from 4.1 to 24.8 years were assessed in total 962 times (mean interval ≈ 1.8 years). The California Verbal Learning Test (CVLT) and the Rey Complex Figure Test (CFT) were used. Recall was tested 30 min and ≈ 10 days after encoding. We found unique developmental effects on recall in the extended retention interval condition independently of 30 min recall performance. For CVLT, major improvements happened between 10 and 15 years. For CFT, improvement was linear and was accounted for by visuo-constructive abilities. The relationships did not show anterior-posterior hippocampal axis differences. In conclusion, performance on recall tests using extended retention intervals shows unique development, likely due to changes in encoding depth or efficacy, or improvements of long-term consolidation processes.
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http://dx.doi.org/10.1016/j.dcn.2019.100723DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974909PMC
December 2019

Age-Related Differences in Functional Asymmetry During Memory Retrieval Revisited: No Evidence for Contralateral Overactivation or Compensation.

Cereb Cortex 2020 03;30(3):1129-1147

Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0317 Oslo, Norway.

Brain asymmetry is inherent to cognitive processing and seems to reflect processing efficiency. Lower frontal asymmetry is often observed in older adults during memory retrieval, yet it is unclear whether lower asymmetry implies an age-related increase in contralateral recruitment, whether less asymmetry reflects compensation, is limited to frontal regions, or predicts neurocognitive stability or decline. We assessed age-related differences in asymmetry across the entire cerebral cortex, using functional magnetic resonance imaging data from 89 young and 76 older adults during successful retrieval, and surface-based methods allowing direct homotopic comparison of activity between cortical hemispheres . An extensive left-asymmetric network facilitated retrieval in both young and older adults, whereas diverse frontal and parietal regions exhibited lower asymmetry in older adults. However, lower asymmetry was not associated with age-related increases in contralateral recruitment but primarily reflected either less deactivation in contralateral regions reliably signaling retrieval failure in the young or lower recruitment of the dominant hemisphere-suggesting that functional deficits may drive lower asymmetry in older brains, not compensatory activity. Lower asymmetry predicted neither current memory performance nor the extent of memory change across the preceding ~ 8 years in older adults. Together, these findings are inconsistent with a compensation account for lower asymmetry during retrieval and aging.
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http://dx.doi.org/10.1093/cercor/bhz153DOI Listing
March 2020

Corticosteroids and Regional Variations in Thickness of the Human Cerebral Cortex across the Lifespan.

Cereb Cortex 2020 03;30(2):575-586

Bordeaux Population Health Research Center, INSERM UMR, University of Bordeaux, Bordeaux 33076, France.

Exposures to life stressors accumulate across the lifespan, with possible impact on brain health. Little is known, however, about the mechanisms mediating age-related changes in brain structure. We use a lifespan sample of participants (n = 21 251; 4-97 years) to investigate the relationship between the thickness of cerebral cortex and the expression of the glucocorticoid- and the mineralocorticoid-receptor genes (NR3C1 and NR3C2, respectively), obtained from the Allen Human Brain Atlas. In all participants, cortical thickness correlated negatively with the expression of both NR3C1 and NR3C2 across 34 cortical regions. The magnitude of this correlation varied across the lifespan. From childhood through early adulthood, the profile similarity (between NR3C1/NR3C2 expression and thickness) increased with age. Conversely, both profile similarities decreased with age in late life. These variations do not reflect age-related changes in NR3C1 and NR3C2 expression, as observed in 5 databases of gene expression in the human cerebral cortex (502 donors). Based on the co-expression of NR3C1 (and NR3C2) with genes specific to neural cell types, we determine the potential involvement of microglia, astrocytes, and CA1 pyramidal cells in mediating the relationship between corticosteroid exposure and cortical thickness. Therefore, corticosteroids may influence brain structure to a variable degree throughout life.
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http://dx.doi.org/10.1093/cercor/bhz108DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444740PMC
March 2020

Error processing in the adolescent brain: Age-related differences in electrophysiology, behavioral adaptation, and brain morphology.

Dev Cogn Neurosci 2019 08 25;38:100665. Epub 2019 May 25.

PROMENTA Research Center, Department of Psychology, University of Oslo, Oslo, Norway; NORMENT, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Psychiatry, Diakonhjemmet Hospital, Oslo, Norway.

Detecting errors and adjusting behaviour appropriately are fundamental cognitive abilities that are known to improve through adolescence. The cognitive and neural processes underlying this development, however, are still poorly understood. To address this knowledge gap, we performed a thorough investigation of error processing in a Flanker task in a cross-sectional sample of participants 8 to 19 years of age (n = 98). We examined age-related differences in event-related potentials known to be associated with error processing, namely the error-related negativity (ERN) and the error positivity (Pe), as well as their relationships with task performance, post-error adjustments and regional cingulate cortex thickness and surface area. We found that ERN amplitude increased with age, while Pe amplitude remained constant. A more negative ERN was associated with higher task accuracy and faster reaction times, while a more positive Pe was associated with higher accuracy, independently of age. When estimating post-error adjustments from trials following both incongruent and congruent trials, post-error slowing and post-error improvement in accuracy both increased with age, but this was only found for post-error slowing when analysing trials following incongruent trials. There were no age-independent associations between either ERN or Pe amplitude and cingulate cortex thickness or area measures.
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http://dx.doi.org/10.1016/j.dcn.2019.100665DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6969341PMC
August 2019
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