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Rashid Deane

Researcher at University of Rochester

Publications -  84
Citations -  23923

Rashid Deane is an academic researcher from University of Rochester. The author has contributed to research in topics: Blood–brain barrier & Glymphatic system. The author has an hindex of 50, co-authored 81 publications receiving 19439 citations. Previous affiliations of Rashid Deane include State University of New York System & University of Rochester Medical Center.

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Journal ArticleDOI

A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β.

TL;DR: An anatomically distinct clearing system in the brain that serves a lymphatic-like function is described and may have relevance for understanding or treating neurodegenerative diseases that involve the mis-accumulation of soluble proteins, such as amyloid β in Alzheimer's disease.
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Sleep Drives Metabolite Clearance From the Adult Brain

TL;DR: It is reported that sleep has a critical function in ensuring metabolic homeostasis and convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep, suggesting the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.
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Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging.

TL;DR: It is shown that age-dependent vascular damage in pericyte-deficient mice precedes neuronal degenerative changes, learning and memory impairment, and the neuroinflammatory response, and pericytes control key neurovascular functions that are necessary for proper neuronal structure and function.
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Apolipoprotein E controls cerebrovascular integrity via cyclophilin A

TL;DR: It is shown that the vascular defects in Apoe-deficient and APOE4-expressing mice precede neuronal dysfunction and can initiate neurodegenerative changes, which suggest that CypA is a key target for treating APoe4-mediated neurovascular injury and the resulting neuronal Dysfunction and degeneration.