Primary and secondary thiamine deficits disturb cholinergic transmission in the brain, impairing the cognitive and motor functions in affected individuals (Gibson et al., 1982; Butterworth, 2009; Jankowska-Kulawy et al., 2010). Thiamine-deficient rats displayed inhibition of ACh synthesis and release, despite the unchanged activities of ChAT – indicating the preservation of cholinergic neurons integrity in these conditions. Thus, TD-evoked inhibition of ACh metabolism resulted exclusively from in situ inhibition of pyruvate oxidation by PDHC, yielding decreased availability of acetyl-CoA in the mitochondria and its secondary deficits in the ACh synthesizing compartment. (Figures 1A,E,,FF). In these conditions, the rate of ACL-dependent fraction of ACh synthesis/release fell from 0.52 to 0.26% of maximal ChAT activity (Jankowska-Kulawy et al., 2010).
Excerpt from:
The Regulatory Effects of Acetyl-CoA Distribution in the Healthy and Diseased Brain. - glucose 2018.
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Cholinergic dysfunction in Parkinson's Disease:
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