Age and Alzheimer's pathology disrupt default mode network functioning via alterations in white matter microstructure but not hyperintensities.
Age and Alzheimer's pathology disrupt default mode network functioning via alterations in white matter microstructure but not hyperintensities.
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DOI：
10.1016/j.cortex.2018.04.006
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发表时间：
2018-07
期刊：
影响因子：
--
通讯作者：
Gold BT
中科院分区：
文献类型：
--
作者：
Brown CA;Jiang Y;Smith CD;Gold BT
默认模式网络（DMN）由特定的大脑区域组成，这些区域负责内部导向的思维过程。任务诱发的DMN失活的减少与年龄增长和执行任务表现较差有关，但这些功能变化的潜在因素尚不清楚。我们研究了白质（WM）微观结构、WM高强度（WMH）和阿尔茨海默病病理对DMN功能年龄相关改变的贡献。35名认知正常的老年人和29名年轻人进行了工作记忆任务fMRI和弥散张量成像。在老年人中，我们测量了脑脊液tau和Aβ42 （AD病理标志物），以及FLAIR成像上的WMH（脑血管疾病标志物）。我们确定了一组显示DMN失活的区域和一组相互连接的WM束（DMN-WM），这两个年龄组都有。在老年人中，DMN失活与任务表现之间存在负相关，这与先前的研究一致。DMN失活减少与AD病理和WM结构有关，但与WMH体积无关。中介分析表明，WM微结构介导DMN失活的下降与衰老和AD病理相关。综上所述，这些结果表明，AD病理可能对WM微观结构施加“二次打击”，超过年龄的影响，两者都有助于老年人DMN失活的减少。
The default mode network (DMN) comprises defined brain regions contributing to internally-directed thought processes. Reductions in task-induced deactivation in the DMN have been associated with increasing age and poorer executive task performance, but factors underlying these functional changes remain unclear. We investigated contributions of white matter (WM) microstructure, WM hyperintensities (WMH) and Alzheimer's pathology to age-related alterations in DMN function. Thirty-five cognitively normal older adults and 29 younger adults underwent working memory task fMRI and diffusion tensor imaging. In the older adults, we measured cerebrospinal fluid tau and Aβ42 (markers of AD pathology), and WMH on FLAIR imaging (marker of cerebrovascular disease). We identified a set of regions showing DMN deactivation and a set of inter-connecting WM tracts (DMN-WM) common to both age groups. There were negative associations between DMN deactivation and task performance in older adults, consistent with previous studies. Decreased DMN deactivation was associated with AD pathology and WM microstructure but not with WMH volume. Mediation analyses showed that WM microstructure mediated declines in DMN deactivation associated with both aging and AD pathology. Together these results suggest that AD pathology may exert a “second-hit” on WM microstructure, over-and-above the effects of age, both contributing to diminished DMN deactivation in older adults.
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影响因子：
3.2
作者：
Grady, CL;Springer, MV;Winocur, G
通讯作者：
Winocur, G
影响因子：
3.7
作者：
Daselaar, Sander M.;Iyengar, Vijeth;Cabeza, Roberto E.
通讯作者：
Cabeza, Roberto E.
DOI：
10.1098/rstb.2005.1634
发表时间：
2005-05-29
影响因子：
6.3
作者：
Beckmann, CF;DeLuca, M;Smith, SM
通讯作者：
Smith, SM
影响因子：
4.2
作者：
Gold BT;Zhu Z;Brown CA;Andersen AH;LaDu MJ;Tai L;Jicha GA;Kryscio RJ;Estus S;Nelson PT;Scheff SW;Abner E;Schmitt FA;Van Eldik LJ;Smith CD
通讯作者：
Smith CD
影响因子：
4.2
作者：
Bartzokis G
通讯作者：
Bartzokis G