Alteration of Vascular Endothelial Cadherin in Alzheimer's Disease Patient and Mouse Model
- Alteration of Vascular Endothelial Cadherin in Alzheimer's Disease Patient and Mouse Model
- 류훈; 조선정; 임현정; 석지웅; 이대훈; 조철만; 조상미; 박문호; 한창수; Neil Kowall; Rudolph E. Tanzi; 고영호
- Issue Date
- VOL 게재예정, 게재예정
- Alzheimer's disease (AD) is characterized by amyloid plaques and pathologic cerebrovascular remodeling. Cerebrovascular abnormalities may contribute to the pathology of AD, but the molecular mechanisms are not fully understood. In this study, we evaluated blood-brain barrier (BBB) disruption and the role of VE-cadherin in the progression of amyloid pathology. Here, we determined that levels of VE-cadherin are decreased in brain vessels of AD patients and mouse model of AD. In vitro experiments showed that the disappearance of VE-cadherin by beta-amyloid at the endothelial cell surface was due to cleavage of VE-cadherin. The disappearance of VE-cadherin in brain vessels was also seen in amyloid precursor protein transgenic mice. In the postmortem brain of individuals with AD, furthermore, levels of VE-cadherin were significantly reduced in vessels. Dementia patients showed a distinct blood biochemical profile characterized by high soluble VE-cadherin (sVEC). There was a strong association between plasma sVEC (adjusted odds ratio = 3.41, P < 0.001) and dementia. These results suggest that measurements of plasma VE-cadherin could have the potential for predicting the risk of progressive AD.
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