Abstract
Preclinical data suggest that cholinergic precursors such as choline or lecithin, increase levels of acetylcholine in specific brain structures, and under certain conditions may enhance cholinergic neurotransmission. A variety of neuropsychiatric diseases including tardive dyskinesia. Huntington's chorea, ataxias, Tourette's syndrome, schizophrenia, affective illness, and senile dementia of the Alzheimer type, has been implicated with a general underactivity of central cholinergic mechanisms. Recent studies have investigated the possibility that cholinergic precursor loading strategies may provide viable treatments for these disorders of presumed cholinergic underactivity. Extensive data demonstrate that the symptoms of tardive dyskinesia can be reduced by choline or lecithin, whereas investigations in other disorders have met with mild success, at best, or are still in preliminary stages. Further controlled studies with choline or lecithin using broader dose ranges, longer durations of treatment, and concomitant administration of agents which may increase the release of acetylcholine are warranted.
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