Adequate availability of choline has been proposed to enable sufficient ACh (1) synthesis for neurotransmission. Precursors of ACh (e.g. choline and lecithin) have been investigated for their effects on synthesis and release of ACh, with a view to increasing ACh release and cholinergic activity. Few clinical or animal studies have reported any significant beneficial effects on cognitive function with these compounds . Therapy failure may be due to impaired uptake mechanisms of choline causing the reduction in ACh synthesis, and not due to insufficient choline supply. This is apparent as it has been reported that more choline occurs in the cerebrospinal fluid of AD patients than in patients without AD, and that choline levels increase with disease progression [8, 19]. Therapy with ACh precursors may be limited by side-effects, including gastrointestinal disturbances such as nausea, vomiting and diarrhoea.
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