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Cerebrovascular pathology in Alzheimer's disease and leukoaraiosis
W R Brown1, D M Moody, C R Thore
1Department of Radiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA. brownb@rad.wfubmc.edu
Insights
Alzheimer
Area of Science:
- Neuroscience
- Pathology
- Cerebrovascular Disease
Background:
- Alzheimer's disease (AD) often presents with white matter degeneration, termed leukoaraiosis (LA), linked to chronic ischemia.
- Periventricular veins in the elderly show collagen accumulation, excessive in LA lesions.
Observation:
- Collagen deposition in periventricular veins is pronounced in LA lesions.
- LA lesions exhibit significant oligodendrocyte apoptosis without inflammation.
- Early amyloid deposits are observed around capillaries in AD brains.
Findings:
- Chronic ischemia leads to leukoaraiosis (LA) in Alzheimer's disease (AD) brains.
- Excessive collagen deposition in periventricular veins contributes to LA.
- Oligodendrocyte apoptosis, not inflammation, characterizes LA lesions.
Implications:
- Understanding collagen's role in LA may reveal new therapeutic targets for AD.
- Investigating the link between vascular pathology and neurodegeneration is crucial for AD research.
- Further research into early amyloid deposition mechanisms in AD is warranted.
Abstract:
A high percentage of patients with Alzheimer's disease (AD) show evidence of white matter degeneration known as leukoaraiosis (LA), which is due to chronic ischemia. We found that the periventricular veins tend to become occluded by multiple layers of collagen in the vessel walls in the elderly. This collagen deposition is particularly excessive in LA lesions. Therefore, it is present in the brains of many AD patients, along with other ischemia-causing cerebrovascular pathology. We found evidence that there is severe loss of oligodendrocytes in LA, due to extensive apoptosis. No evidence of inflammation was found in the LA lesions. In thick celloidin sections of AD brain, we have obtained detailed 3D views of small (early) deposits of amyloid (stained with beta-amyloid antibody) around capillaries (stained with collagen IV antibody).