Abstract
Accumulation, aggregation and deposition of the amyloid-β (Aβ) peptides in the brain are widely accepted as the central events in the pathogenesis of Alzheimer's disease (AD). Any factor that is capable of causing these events is potentially a risk factor for AD. In the last decade, evidence has accumulated to support the association between cerebral vascular diseases (CVD) and AD. CVD is known to induce amyloid deposition and affects the age of onset for sporadic AD; whereas, amyloid deposition has been shown to cause cerebrovascular degeneration. In this review, we propose a positive feedback loop between CVD and amyloid deposition. The disease cycle could be triggered by aging and/or other environmental factor-associated CVD, as in late-onset sporadic AD patients, or by over production of Aβ, as in the familial AD patients and amyloid precursor protein transgenic animals.
Keywords: Cerebral amyloid angiopathy, blood-brain barrier, hemorrhage, ischemia, hypoperfusion.
Current Alzheimer Research
Title:Cerebrovascular Pathology and Amyloid Plaque Formation in Alzheimer’s Disease
Volume: 11 Issue: 1
Author(s): Chu-Wan Lee, Yao-Hsiang Shih and Yu-Min Kuo
Affiliation:
Keywords: Cerebral amyloid angiopathy, blood-brain barrier, hemorrhage, ischemia, hypoperfusion.
Abstract: Accumulation, aggregation and deposition of the amyloid-β (Aβ) peptides in the brain are widely accepted as the central events in the pathogenesis of Alzheimer's disease (AD). Any factor that is capable of causing these events is potentially a risk factor for AD. In the last decade, evidence has accumulated to support the association between cerebral vascular diseases (CVD) and AD. CVD is known to induce amyloid deposition and affects the age of onset for sporadic AD; whereas, amyloid deposition has been shown to cause cerebrovascular degeneration. In this review, we propose a positive feedback loop between CVD and amyloid deposition. The disease cycle could be triggered by aging and/or other environmental factor-associated CVD, as in late-onset sporadic AD patients, or by over production of Aβ, as in the familial AD patients and amyloid precursor protein transgenic animals.
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Cite this article as:
Lee Chu-Wan, Shih Yao-Hsiang and Kuo Yu-Min, Cerebrovascular Pathology and Amyloid Plaque Formation in Alzheimer’s Disease, Current Alzheimer Research 2014; 11 (1) . https://dx.doi.org/10.2174/1567205010666131119234308
DOI https://dx.doi.org/10.2174/1567205010666131119234308 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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