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Updated: May 18, 2026

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
Published on: October 30, 2018
Neurovascular dysfunction and faulty amyloid β-peptide clearance in Alzheimer disease
Abhay P Sagare1, Robert D Bell, Berislav V Zlokovic
1Center for Neurodegenerative and Vascular Brain Disorders and Interdisciplinary Program in Dementia Research, Arthur Kornberg Medical Research Building, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA.
Abstract:
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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