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Cerebrovascular muscle atrophy is a feature of Alzheimer's disease
G Perry1, M A Smith, C E McCann
1Institute of Pathology, 2085 Adelbert Road, Case Western Reserve University, Cleveland, OH 44106, USA. gxp7@po.cwru.edu
Abstract:
We examined vascular amyloid-beta deposition and other abnormalities in the posterior cerebral artery of consecutive cases of Alzheimer's disease (AD) compared to controls. Smooth muscle atrophy was a consistent feature in the cases of AD examined (p<0.01) and was surprisingly independent of adjacent amyloid-beta deposition. These findings suggest that vascular abnormalities are a consistent feature in AD and may be an important contributor to the pathogenesis and complications of AD.
Insights
Vascular abnormalities, including smooth muscle atrophy, are consistently found in Alzheimer's disease (AD) brains, independent of amyloid-beta. These vascular changes may contribute to AD development and complications.
Area of Science:
- Neurology
- Pathology
- Vascular Biology
Background:
- Alzheimer's disease (AD) is a neurodegenerative disorder.
- Cerebrovascular abnormalities are increasingly recognized in AD pathogenesis.
Purpose of the Study:
- To investigate vascular amyloid-beta deposition and other abnormalities in the posterior cerebral artery in Alzheimer's disease (AD).
- To determine the relationship between vascular abnormalities and amyloid-beta deposition in AD.
Main Methods:
- Examination of posterior cerebral artery samples from consecutive cases of Alzheimer's disease (AD) and control subjects.
- Histopathological analysis to assess vascular amyloid-beta deposition and smooth muscle integrity.
Main Results:
- Smooth muscle atrophy was a consistent feature in the posterior cerebral arteries of AD cases (p<0.01).
- Smooth muscle atrophy was observed independently of adjacent amyloid-beta deposition.
Conclusions:
- Vascular abnormalities, particularly smooth muscle atrophy, are a consistent feature in Alzheimer's disease (AD).
- These vascular changes may play a significant role in the pathogenesis and complications of AD.