• P B Forgacs and I Bodis-Wollner.
• Department of Neurology, State University of New York, Downstate Medical Center, and Parkinson's Disease and Related Disorders Clinic, Center of Excellence, Kings County Hospital Center and SUNY, Brooklyn, NY 11203, USA.
• J Neural Transm. 2004 Oct 1; 111 (10-11): 1317-31.

AbstractParkinson's Disease (PD) is associated with cognitive deficits. The earliest impairment is evident for executive abilities, visuospatial orientation and memory. Dopamine deficiency is unlikely to be singly responsible for all cognitive changes in PD. Acetyl-choline has an essential role in cognition, thus cholinergic transmission may have an important role in non-dopaminergic cognitive changes. If so, some cognitive defects could possibly be treated with choline-esterase inhibitors. A concern is the potential negative motor effect of cholinergic medication in PD. Surprisingly, these are reported only in a few patients studied. Establishing the relationship between select cognitive deficits and nicotinic neurotransmission may lay the foundation for rational pharmacotherapy of cognitive dysfunction in PD. We summarize anatomical, physiological and pharmacological aspects of nicotinic receptor function. The focus is on those nicotine receptor dependent cognitive dysfunctions which are likely to contribute to motor impairment. Lastly, we discuss hypotheses concerning cholinergic involvement in neuronal synchrony and sensorimotor integration in PD.

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