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Cited by 52Alzheimer's disease research and treatmentsBarrier Structure and Function StudiesNeurological Disease Mechanisms and Treatments

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Cortical Cholinergic Denervation Elicits Vascular Aβ Deposition

ROHER, ALEX E., KUO, YU‐MIN, POTTER, PAMELA E., EMMERLING, MARK R., DURHAM, ROBERT A., WALKER, DOUGLAS G., SUE, LUCIA I., HONER, WILLIAM G., BEACH, THOMAS G.·2000·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2000.tb06388.x
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Abstract

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.

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Crossref · 10.1111/j.1749-6632.2000.tb06388.x

Cites

4 of 4 references verified0 citation errors · 0 not checkable

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  • The mechanism by which anticholinergic medications might contribute to dementia risk is biologically plausible.

    “The mechanism by which anticholinergic medications might contribute to dementia risk has not been elucidated; however, a few lines of evidence suggest that it is biologically plausible.”

    From Cumulative Use of Strong Anticholinergics and Incident Dementia: A Prospective Cohort Study (2015) · cites this paper as [40]

  • In animal models, reduced cholinergic transmission via atropine or cortical cholinergic denervation increased amyloid beta concentrations.

    “Moreover, in animal models, reduced cholinergic transmission via atropine or cortical cholinergic denervation increased amyloid beta concentrations.38-40”

    From Cumulative Use of Strong Anticholinergics and Incident Dementia: A Prospective Cohort Study (2015) · cites this paper as [40]

Citations

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Metadata

Authors
ROHER, A. E., KUO, Y., POTTER, P. E., EMMERLING, M. R., DURHAM, R. A., WALKER, D. G., SUE, L. I., HONER, W. G., & BEACH, T. G.
Affiliations
  • Banner Sun Health Research Institute (US)
  • University of British Columbia (CA)
Corresponding author
ROHER, ALEX E.
ORCID
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2000-04
Volume
903
Issue
1
Pages
366-373
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2000.tb06388.x
OpenAlex
W2084120977
Cited by
52
References
4
Citations by year
2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 5 · 2020: 3 · 2018: 1 · 2017: 3 · 2016: 2 · 2015: 4 · 2014: 1 · 2013: 2 · 2012: 1
FWCI
0.70
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2130 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
amyloid-beta deposition, nucleus basalis magnocellularis, cholinergic denervation, saporin, p75 neurotrophin receptor, acetylcholine, vasodilation, cerebral hypoperfusion, blood-brain barrier, Alzheimer's disease model, cerebral blood flow
MeSH terms
Saporins, Acetylcholine, Alzheimer Disease, Animals, Antibodies, Monoclonal, Immunotoxins, Blood-Brain Barrier, Cerebral Cortex, Cerebral Ventricles, Cerebrovascular Circulation, Denervation, Immunoglobulin G, Injections, Intraventricular, Functional Laterality, Microcirculation, N-Glycosyl Hydrolases, Plant Proteins, Rabbits, Regional Blood Flow, Amyloid beta-Peptides, Receptors, Nerve Growth Factor, Basal Nucleus of Meynert, Ribosome Inactivating Proteins, Type 1

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