Genetics of subcortical vascular dementia

被引：31

作者：

Schmidt, Helena ^{[1
,2
]}

Freudenberger, Paul ^{[1
]}

Seiler, Stephan ^{[3
]}

Schmidt, Reinhold ^{[3
]}

机构：

[1] Med Univ Graz, Inst Mol Biol & Biochem, Ctr Mol Med, A-8010 Graz, Austria

[2] Med Univ Graz, Dept Neurol, Clin Sect Gen Neurol, A-8036 Graz, Austria

[3] Med Univ Graz, Dept Neurol, Clin Sect Neurogeriatr, A-8036 Graz, Austria

来源：

EXPERIMENTAL GERONTOLOGY | 2012年 / 47卷 / 11期

基金：

奥地利科学基金会;

关键词：

Subcortical vascular dementia cerebral small vessel disease; Genetics; White matter lesions; Lacunes; Microbleeds; Risk factors; SMALL-VESSEL DISEASE; WHITE-MATTER HYPERINTENSITY; AUSTRIAN STROKE PREVENTION; HYPERTENSIVE SIBSHIPS; CEREBRAL MICROBLEEDS; LESION VOLUME; RISK-FACTORS; BRAIN; NOTCH3; LEUKOARAIOSIS;

D O I：

10.1016/j.exger.2012.06.003

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Subcortical vascular dementia or cerebral small vessel disease is a common cause of disability in the elderly. On magnetic resonance imaging the disease is manifested as white matter lesions, lacunes and microbleeds. Its etiology is complex, with age and hypertension as established risk factors. The heritability of white matter lesions is constantly high over different populations. Linkage studies identified several loci for these lesions however no genes responsible for the linkage signals had been identified so far. Results from genetic association studies using the candidate gene approach support the role of APOE, the renin-angiotensin system, as well as the Notch3 signaling pathway in the development of subcortical vascular dementia. The recent genomegenome wide association study on white matter lesions identified a novel locus on chromosome 17q25 harboring several genes such as TRIM65 and TRIM47 which pinpoints to possible novel mechanisms leading to these lesions. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：873 / 877

页数：5

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