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Cortical Cholinergic Denervation Elicits Vascular Aβ Deposition
Author(s) -
ROHER ALEX E.,
KUO YUMIN,
POTTER PAMELA E.,
EMMERLING MARK R.,
DURHAM ROBERT A.,
WALKER DOUGLAS G.,
SUE LUCIA I.,
HONER WILLIAM G.,
BEACH THOMAS G.
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06388.x
Subject(s) - cholinergic , nucleus basalis , acetylcholine , denervation , cholinergic neuron , blood–brain barrier , endocrinology , chemistry , cerebral blood flow , neuroscience , medicine , biology , central nervous system
A bstract : Selective destruction of the cholinergic nucleus basalis magnocellularis (nbm) in the rabbit by the p75 neurotrophin receptor (NTR) immunoglobulin G (IgG) complexed to the toxin saporin leads to the deposition of amyloid‐beta (Aβ) in and around cerebral blood vessels. In some instances, the perivascular Aβ resemble the diffuse deposits observed in Alzheimer's disease (AD). We propose that cortical cholinergic deprivation results, among other perturbations, in the loss of vasodilation mediated by acetylcholine. In addition to a dysfunctional cerebral blood flow, alterations in vascular chemistry affecting endothelial and smooth muscle cells may result in cerebral hypoperfusion and a breached blood‐brain barrier (BBB). The selective removal of the rabbit nbm and Aβ accumulation may serve as an important nontransgenic, and more physiological, model for the testing of pharmacological and immunological agents designed to control the deposition and the deleterious effects of Aβ in AD.