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From the Departments of Neurology and Psychiatry & Biobehavioral Sciences, UCLA School of Medicine, and the Behavioral Neuroscience Section, Psychiatry Service, West Los Angeles Veterans Affairs Medical Center, Los Angeles, CA (Dr. Cummings), and the Departments of Psychiatry and Neurology, University of Pittsburgh, Pittsburgh, PA (Dr. Kaufer).
The authors have served as consultants or have engaged in research sponsored by Parke-Davis, Eli Lilly, Pfizer, Sandoz, Bayer, Merck-Dupont, Sigma-Tau, and Glaxo pharmaceutical companies.
Received January 11, 1996. Accepted in final form March 15, 1996.
Address correspondence and reprint requests to Dr. Jeffrey L. Cummings, Reed Neurological Research Center, UCLA School of Medicine, 710 Westwood Plaza, Los Angeles, CA 90024.
Altered cholinergic function is a prominent feature of AD.The neuropsychological impairments of AD are attributed, at least partially, to the cholinergic disturbance, and current approaches to treatment of the cognitive abnormalities attempt to enhance cholinergic function. Behavioral changes are common in AD and include psychosis, agitation, depression, anxiety, personality alterations, and neurovegetative changes. The contribution of the cholinergic deficiency to the behavioral alterations has been little explored, but neurochemical, neuroanatomic, pharmacologic, and clinical observations suggest that the cholinergic deficiency contributes importantly to the neuropsychiatric dimension of AD. Investigation of the role of cholinergic dysfunction in the behavioral changes of AD will improve understanding of the pathophysiologic basis of these abnormalities and may lead to new types of therapy for the neuropsychiatric disturbances associated with this common dementing disorder.
NEUROLOGY 1996;47: 876-883
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