Cortical cholinergic denervation elicits vascular Aβ deposition

Alex E. Roher, Yu Min Kuo, Pamela E. Potter, Mark R. Emmerling, Robert A. Durham, Douglas G. Walker, Lucia I. Sue, William G. Honer, Thomas G. Beach

Research output: Contribution to journalArticlepeer-review

41 Citations (Scopus)


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 now, 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.

Original languageEnglish
Pages (from-to)366-373
Number of pages8
JournalAnnals of the New York Academy of Sciences
Publication statusPublished - 2000 Jan 1

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science


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