Gray matter network associated with risk for Alzheimer's disease in young to middle-aged adults.

Gray matter network associated with risk for Alzheimer's disease in young to middle-aged adults.
复制标题

DOI:
10.1016/j.neurobiolaging.2012.01.014
复制
发表时间:
2012-12
影响因子:
4.2
通讯作者:
Moeller JR
Moeller JR
中科院分区:
医学2区
文献类型:
--
作者:
Alexander GE;Bergfield KL;Chen K;Reiman EM;Hanson KD;Lin L;Bandy D;Caselli RJ;Moeller JR

文献摘要

参考文献

被引文献

相似文献

载脂蛋白E(APOE)ε4等位基因会增加迟发性阿尔茨海默病(AD)以及与年龄相关的认知能力下降的风险。我们研究了在可能出现AD痴呆或健康的认知老化之前几十年,与非ε4携带者相比,ε4携带者是否表现出灰质体积的减少。对14名年龄在26岁至45岁之间认知正常的ε4携带者和10名年龄匹配的非ε4携带者进行了T1加权容积磁共振成像(MRI)扫描。所有人都报告有一级或二级痴呆家族病史。使用基于体素的形态测量学(VBM)以及区域协方差的多元模型——缩放子轮廓模型(SSM)来检验灰质的组间差异。前两个SSM MRI灰质模式的组合将APOE ε4携带者与非携带者区分开来。这种组合模式显示双侧背外侧和内侧额叶、前扣带回、顶叶和外侧颞叶皮质的灰质减少,同时小脑、枕叶、梭状回和海马区域有相应的相对增加。由于这些灰质差异在可能出现痴呆或认知老化之前几十年就已出现,结果表明大脑形态存在长期的、与基因相关的差异,这可能导致对迟发性AD或健康大脑老化的后期影响具有优先易感性。
The apolipoprotein E (APOE) ε4 allele increases the risk for late-onset Alzheimer's disease (AD) and age-related cognitive decline. We investigated whether ε4 carriers show reductions in gray matter volume compared to ε4 non-carriers decades prior to the potential onset of AD dementia or healthy cognitive aging. Fourteen cognitively normal ε4 carriers, ages 26 to 45, were compared with 10 age-matched, ε4 non-carriers using T1-weighted volumetric magnetic resonance imaging (MRI) scans. All had reported first or second-degree family histories of dementia. Group differences in gray matter were tested using voxel-based morphometry (VBM) and a multivariate model of regional covariance, the Scaled Subprofile Model (SSM). A combination of the first two SSM MRI gray matter patterns distinguished the APOE ε4 carriers from non-carriers. This combined pattern showed gray matter reductions in bilateral dorsolateral and medial frontal, anterior cingulate, parietal, and lateral temporal cortices with co-varying relative increases in cerebellum, occipital, fusiform, and hippocampal regions. With these gray matter differences occurring decades prior to the potential onset of dementia or cognitive aging, the results suggest longstanding, gene-associated differences in brain morphology that may lead to preferential vulnerability for the later effects of late onset AD or healthy brain aging.
DOI: 10.1016/j.jalz.2009.07.003
发表时间: 2010-07
期刊: Alzheimer's & dementia : the journal of the Alzheimer's Association
影响因子: --
作者:
Dennis NA;Browndyke JN;Stokes J;Need A;Burke JR;Welsh-Bohmer KA;Cabeza R
通讯作者: Cabeza R
DOI: 10.1176/appi.ajp.159.5.738
发表时间: 2002-05-01
影响因子: 17.7
作者:
Alexander, GE;Chen, K;Reiman, EM
通讯作者: Reiman, EM
DOI: 10.1016/s0022-5371(73)80034-9
发表时间: 1973-01-01
期刊: JOURNAL OF VERBAL LEARNING AND VERBAL BEHAVIOR
影响因子: --
作者:
BUSCHKE, H
通讯作者: BUSCHKE, H
DOI: 10.1212/wnl.36.7.879
发表时间: 1986-07-01
期刊: NEUROLOGY
影响因子: 9.9
作者:
DUARA, R;GRADY, C;RAPOPORT, SI
通讯作者: RAPOPORT, SI
DOI: 10.1212/wnl.45.11.1995
发表时间: 1995-11-01
期刊: NEUROLOGY
影响因子: 9.9
作者:
EIDELBERG, D;MOELLER, JR;FAHN, S
通讯作者: FAHN, S