Cerebrovascular smooth muscle actin is increased in nondemented subjects with frequent senile plaques at autopsy: implications for the pathogenesis of Alzheimer disease.


Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Hulette, CM; Ervin, JF; Edmonds, Y; Antoine, S; Stewart, N; Szymanski, MH; Hayden, KM; Pieper, CF; Burke, JR; Welsh-Bohmer, KA

Published Date

  • April 2009

Published In

Volume / Issue

  • 68 / 4

Start / End Page

  • 417 - 424

PubMed ID

  • 19287310

Pubmed Central ID

  • 19287310

International Standard Serial Number (ISSN)

  • 0022-3069

Digital Object Identifier (DOI)

  • 10.1097/NEN.0b013e31819e6334


  • eng

Conference Location

  • England