Cerebrovascular smooth muscle actin is increased in nondemented subjects with frequent senile plaques at autopsy: implications for the pathogenesis of Alzheimer disease.
Cerebrovascular smooth muscle actin is increased in nondemented subjects with frequent senile plaques at autopsy: implications for the pathogenesis of Alzheimer disease.
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在尸检时经常出现老年斑的非痴呆受试者中，脑血管平滑肌肌动蛋白增加：对阿尔茨海默病发病机制的影响。
DOI：
10.1097/nen.0b013e31819e6334
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发表时间：
2009
影响因子：
3.2
通讯作者：
Welsh-Bohmer,KathleenA
中科院分区：
文献类型：
--
作者：
Hulette,ChristineM;Ervin,JohnF;Edmonds,Yvette;Antoine,Samantha;Stewart,Nicolas;Szymanski,MariH;Hayden,KathleenM;Pieper,CarlF;Burke,JamesR;Welsh-Bohmer,KathleenA
我们以前发现，血管平滑肌肌动蛋白（SMA）是减少在晚期阿尔茨海默病（AD）患者的大脑相比，非痴呆，神经病理正常受试者的大脑。为了评估这一发现的发病学意义和疾病特异性，我们研究了另外3个患者组：无显著AD类型病理学的非痴呆受试者（"正常"; n = 20），尸检时频繁出现老年斑的非痴呆受试者（"临床前AD"; n = 20）和额颞叶痴呆受试者（"FTD"; n = 10）。各组的性别和年龄与先前报告的相匹配;如先前所述进行SMA免疫组织化学和图像分析。令人惊讶的是，临床前AD组蛛网膜、大脑皮质和白色小动脉中的SMA表达高于正常组和FTD组。在该组中，斑块与淀粉样血管病或其他血管疾病无关。正常组脑中的平滑肌肌动蛋白表达介于临床前AD和FTD组之间。所有3组的SMA表达均比我们之前的报告中的高得多。非痴呆受试者大脑中频繁斑块和小动脉SMA表达增加的存在表明，SMA表达增加可能代表对神经变性的生理反应，可以预防或延迟AD中的显性表达痴呆。
We previously found that vascular smooth muscle actin (SMA) is reduced in the brains of patients with late stage Alzheimer disease (AD) compared with brains of nondemented, neuropathologically normal subjects. To assess the pathogenetic significance and disease specificity of this finding, we studied 3 additional patient groups: nondemented subjects without significant AD type pathology ("Normal"; n = 20), nondemented subjects with frequent senile plaques at autopsy ("Preclinical AD"; n = 20), and subjects with frontotemporal dementia ("FTD"; n = 10). The groups were matched for sex and age with those previously reported; SMA immunohistochemistry and image analysis were performed as previously described. Surprisingly, SMA expression in arachnoid, cerebral cortex, and white matter arterioles was greater in the Preclinical AD group than in the Normal and FTD groups. The plaques were not associated with amyloid angiopathy or other vascular disease in this group. Smooth muscle actin expression in the brains of the Normal group was intermediate between the Preclinical AD and FTD groups. All 3 groups exhibited much greater SMA expression than in our previous report. The presence of frequent plaques and increased arteriolar SMA expression in the brains of nondemented subjects suggest that increased SMA expression might represent a physiological response to neurodegeneration that could prevent or delay overt expression dementia in AD.