Fix: Glucose, acetyl-CoA, Thiamine, cholinergics, Parkinson's, acetylcholine

[aspergerian]

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.

ncbi.nlm.nih.gov/pmc/articl...

Cholinergic dysfunction in Parkinson's Disease:

ncbi.nlm.nih.gov/pmc/articl...

ncbi.nlm.nih.gov/pmc/articl...

ncbi.nlm.nih.gov/pmc/articl...

[WinnieThePoo]

your references to the source articles are not useable. Can you relink please?

[aspergerian in reply to WinnieThePoo]

Try the links in:

healthunlocked.com/parkinso...