期刊
ALZHEIMERS & DEMENTIA
卷 8, 期 6, 页码 574-583出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jalz.2011.05.2429
关键词
Alzheimer's disease; Amyloid-beta; Brain microvasculature; Brain microhemorrhages; Brain hypoperfusion
资金
- National Institute on Aging [R01 AG019795, R21 AG035078]
- State of Arizona Alzheimer Disease Research Consortium
Here, we synthesize several lines of evidence supporting the hypothesis that at least one function of amyloid-beta is to serve as a part of the acute response to brain hemodynamic disturbances intended to seal vascular leakage. Given the resilient and adhesive physicochemical properties of amyloid, an abluminal hemostatic repair system might be highly advantageous, if deployed on a limited and short-term basis, in young individuals. However, in the aged, inevitable cardiovascular dysfunction combined with brain microvascular lesions may yield global chronic hypoperfusion that may lead to continuous amyloid deposition and consequential negative effects on neuronal viability. A large body of experimental evidence supports the hypothesis of an amyloid-beta rescue function gone astray. Preventing or inducing the removal of amyloid in Alzheimer's disease (AD) has been simultaneously successful and disappointing. Amyloid deposits clearly play major roles in AD, but they may not represent the preeminent factor in dementia pathogenesis. Successful application of AD preventative approaches may hinge on an accurate and comprehensive view of comorbidities, including cardiovascular disease, diabetes, and head trauma. (C) 2012 The Alzheimer's Association. All rights reserved.
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