Neurovascular Dysfunction and Faulty Amyloid -Peptide Clearance in Alzheimer Disease
Author(s) -
Abhay P. Sagare,
Robert D. Bell,
Berislav V. Zloković
Publication year - 2012
Publication title -
cold spring harbor perspectives in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.853
H-Index - 105
eISSN - 2472-5412
pISSN - 2157-1422
DOI - 10.1101/cshperspect.a011452
Subject(s) - neurovascular bundle , pathogenesis , medicine , cerebral blood flow , neuroscience , alzheimer's disease , blood–brain barrier , amyloid (mycology) , disease , cerebral circulation , pathology , cardiology , biology , central nervous system
Neurovascular dysfunction is an integral part of Alzheimer disease (AD). Changes in the brain vascular system may contribute in a significant way to the onset and progression of cognitive decline and the development of a chronic neurodegenerative process associated with accumulation of amyloid β-peptide (Aβ) in brain and cerebral vessels in AD individuals and AD animal models. Here, we review the role of the neurovascular unit and molecular mechanisms in cerebral vascular cells behind the pathogenesis of AD. In particular, we focus on blood-brain barrier (BBB) dysfunction, decreased cerebral blood flow, and impaired vascular clearance of Aβ from brain. The data reviewed here support an essential role of the neurovascular and BBB mechanisms in AD pathogenesis.
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