期刊论文详细信息
NEUROBIOLOGY OF AGING 卷:96
Increased functional homotopy of the prefrontal cortex is associated with corpus callosum degeneration and working memory decline
Article
Avelar-Pereira, Barbara1,2,3  Backman, Lars1,2  Wahlin, Anders3,4  Nyberg, Lars3,4,5  Salami, Alireza1,2,3,4,5,6 
[1] Karolinska Inst, Aging Res Ctr, Tomtebodavagen 18A, S-17165 Stockholm, Sweden
[2] Stockholm Univ, Stockholm, Sweden
[3] Umea Univ, Umea Ctr Funct Brain Imaging, Umea, Sweden
[4] Umea Univ, Dept Radiat Sci, Umea, Sweden
[5] Umea Univ, Dept Integrat Med Biol, Umea, Sweden
[6] Umea Univ, Wallenberg Ctr Mol Med, Umea, Sweden
关键词: Aging;    Homotopic connectivity;    Resting-state fMRI;    Longitudinal;    DTI;    White matter;    Corpus callosum;    Working memory;   
DOI  :  10.1016/j.neurobiolaging.2020.08.008
来源: Elsevier
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【 摘 要 】

Functional homotopy reflects the link between spontaneous activity in a voxel and its counterpart in the opposite hemisphere. Alterations in homotopic functional connectivity (FC) are seen in normal aging, with highest and lowest homotopy being present in sensory-motor and higher-order regions, respectively. Homotopic FC relates to underlying structural connections, but its neurobiological underpinnings remain unclear. The genu of the corpus callosum joins symmetrical parts of the prefrontal cortex (PFC) and is susceptible to age-related degeneration, suggesting that PFC homotopic connectivity is linked to changes in white-matter integrity. We investigated homotopic connectivity changes and whether these were associated with white-matter integrity in 338 individuals. In addition, we examined whether PFC homotopic FC was related to changes in the genu over 10 years and working memory over 5 years. There were increases and decreases in functional homotopy, with the former being prevalent in subcortical and frontal regions. Increased PFC homotopic FC was partially driven by structural degeneration and negatively associated with working memory, suggesting that it reflects detrimental age-related changes. (C) 2020 The Author(s). Published by Elsevier Inc.

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