Cerebrovascular Pathology and Amyloid Plaque Formation in Alzheimer’s Disease

ISSN: 1875-5828 (Online)
ISSN: 1567-2050 (Print)

Volume 14, 12 Issues, 2017

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Current Alzheimer Research

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  • 59th of 192 in Clinical Neurology
  • 101st of 256 in Neurosciences

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Prof. Debomoy K. Lahiri
Department of Psychiatry, Indiana University School of Medicine
Neuroscience Research Center
Indianapolis, IN 46202

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5 - Year: 3.58

Cerebrovascular Pathology and Amyloid Plaque Formation in Alzheimer’s Disease

Current Alzheimer Research, 11(1): 4-10.

Author(s): Chu-Wan Lee, Yao-Hsiang Shih and Yu-Min Kuo.

Affiliation: Department of Cell Biology and Anatomy, National Cheng Kung University. 1 Ta Hsueh Road, Tainan, Taiwan 70101.


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.


Cerebral amyloid angiopathy, blood-brain barrier, hemorrhage, ischemia, hypoperfusion.

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Article Details

Volume: 11
Issue Number: 1
First Page: 4
Last Page: 10
Page Count: 7
DOI: 10.2174/1567205010666131119234308
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