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Idland, A.-V.

Publications and source records attributed to Idland, A.-V..

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

BackgroundPoor 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.\n\nMethodsSelf-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, covering up to 11 years. Cross-sectional analyses were repeated in a sample of 21390 participants from the UK Biobank.\n\nResultsThe relationship between self-reported sleep and age differed across sleep items. Sleep duration, efficiency, problems, and use of medication worsened monotonously with age, whereas subjective sleep quality, sleep latency, and daytime tiredness improved. Women reported worse sleep in general than men, but the relationship to age was similar. No cross-sectional sleep - hippocampal volume relationships was found. However, worse sleep quality, efficiency, problems, and daytime tiredness were related to greater hippocampal volume loss over time, with high scorers showing on average 0.22% greater annual loss than low scorers. Simulations showed that longitudinal effects were too small to be detected as age-interactions in cross-sectional analyses.\n\nConclusionsWorse self-reported sleep is associated with higher rates of hippocampal 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.

neuroscience

Genetic risk for Alzheimer`s disease predicts hippocampal volume through the lifespan

INTRODUCTIONIt is unknown whether genetic risk for Alzheimers disease (AD) represents a stable influence on the brain from early in life, or whether effects are age-dependent. It is critical to characterize the effects of genetic risk factors on the primary neural substrate of AD, the hippocampus, throughout life.\n\nMETHODSRelations of polygenic risk score (PGS) for AD, including variants in Apolipoprotein E (APOE) with hippocampal volume and its change were assessed in a healthy longitudinal lifespan sample (n = 1181, 4-95 years), followed for up to 11 years with a total of 2690 MRI scans.\n\nRESULTSAD-PGS showed a significant negative effect on hippocampal volume. Offset effects of AD-PGS and APOE {varepsilon}4 were present in hippocampal development, and interactions between age and genetic risk on volume change were not consistently observed. DISCUSSION: Endophenotypic manifestation of polygenic risk for AD may be seen across the lifespan in healthy persons.\n\nHighlightsO_LIGenetic risk for AD affects the hippocampus throughout the lifespan\nC_LIO_LIAPOE {varepsilon}4 carriers have smaller hippocampi in development\nC_LIO_LIDifferent effects of genetic risk at different ages were not consistently observed\nC_LIO_LIGenetic factors increasing risk for AD impact healthy persons throughout life\nC_LIO_LIA broader population and age range are relevant targets for attempts to prevent AD\nC_LI

neuroscience