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大脑皮层在成年后的不对称变薄在阿尔茨海默病中加速。

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

机构信息

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

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

出版信息

Nat Commun. 2021 Feb 1;12(1):721. doi: 10.1038/s41467-021-21057-y.

DOI:10.1038/s41467-021-21057-y
PMID:33526780
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7851164/
Abstract

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.

摘要

衰老和阿尔茨海默病(AD)与大脑逐渐紊乱有关。尽管结构不对称是大脑皮层的组织特征,但尚不清楚连续的年龄和 AD 相关皮层退化是否会改变皮层不对称性。在这里,在多个成年人的多个纵向寿命队列中,我们表明,在 20 岁左右表现出明显不对称性的高级皮层区域,在成年期也会出现逐渐的不对称性丧失。因此,(以前)较厚的同源半球的加速变薄是衰老的一个特征。在 Lifebrain 联合组织中,这一组织原则在队列之间具有高度一致性,并且在复制样本中,不对称性丧失的拓扑模式和时间动态都非常相似。AD 中这种变化进一步加速。结果表明,在衰老和 AD 中,异模态皮层的自适应不对称组织出现了系统范围的去分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/5f7b70be447e/41467_2021_21057_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/de417f821134/41467_2021_21057_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/c7aa2744f78d/41467_2021_21057_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/793910c29e77/41467_2021_21057_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/2d80ed847360/41467_2021_21057_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/5f7b70be447e/41467_2021_21057_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/de417f821134/41467_2021_21057_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/c7aa2744f78d/41467_2021_21057_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/793910c29e77/41467_2021_21057_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/2d80ed847360/41467_2021_21057_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dd/7851164/5f7b70be447e/41467_2021_21057_Fig5_HTML.jpg

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