Journal
ALZHEIMERS RESEARCH & THERAPY
Volume 5, Issue 6, Pages -Publisher
BMC
DOI: 10.1186/alzrt230
Keywords
-
Categories
Funding
- Canadian Institutes of Health Research
Ask authors/readers for more resources
Growing evidence suggests that vascular perturbation plays a critical role in the pathogenesis of Alzheimer's disease (AD). It appears to be a common feature in addition to the classic pathological hallmarks of amyloid beta (A beta) plaques and neurofibrillary. Moreover, the accumulation of A beta in the cerebral vasculature is closely associated with cognitive decline, and disruption of the blood-brain barrier (BBB) has been shown to coincide with the onset of cognitive impairment. Although it was originally hypothesized that the accumulation of A beta and the subsequent disruption of the BBB were due to the impaired clearance of A beta from the brain, a body of data now suggests an alternative hypothesis for vascular dysfunction in AD that amyloidogenesis promotes extensive neoangiogenesis leading to increased vascular permeability and subsequent hypervascularization. In this review, we discuss the role A beta plays in angiogenesis of the neurovasculature and BBB and how it may contribute to the pathogenesis of AD. These studies suggest that interventions that directly or indirectly affect angiogenesis could have beneficial effects on amyloid and other pathways in AD.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available