title: Primate models of cholinergic dysfunction.
abstract: Neuropathological studies are currently providing extensive information upon which to base experimental models of neurodegenerative diseases. While it seems unlikely that a single model encompassing all aspects of degenerative dementia will be developed in the near future, models that are more restricted in their scope can provide useful data about processes which range from cellular to behavioral disturbances. In this article we present recent primate studies revealing that mature basal forebrain cholinergic neurons degenerate as a consequence of the removal of their target. Both fimbria fornix transection and cortical devascularization seem to be useful tools in the assessment of potential neurotrophic and neuroprotective properties of pharmacological agents.
authors.affiliation: Department of Pharmacology and Therapeutics, McGill University, Montreal, P.Q., Canada.
authors.forename: P
authors.initials: P
authors.lastname: Liberini
authors.forename: A C
authors.initials: AC
authors.lastname: Cuello
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D000911:Antibodies, Monoclonal; D001927:Brain Diseases / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000502:physiology* / Q000503:physiopathology*; D002795:Choline O-Acetyltransferase / Q000378:metabolism / Q000502:physiology*; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology; D009414:Nerve Growth Factors / Q000494:pharmacology; D011323:Primates; D016548:Prosencephalon / Q000503:physiopathology*; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000502:physiology*
chemical_list: D000911:Antibodies, Monoclonal; D009414:Nerve Growth Factors; D011950:Receptors, Cholinergic; D002795:Choline O-Acetyltransferase; D000110:Acetylcholinesterase