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.
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