GSK3b inactivates PDHC

This could be a cause of developing thiamine dependency - overactive GSK3b inactivates PDHC.

Secondly, acetylcholine synthesis is suppressed by GSK-3β, thus implicating the kinase in the cholinergic deficit characteristic of the disease.

This effect has been shown to be mediated by GSK-3β-dependent inactivation of pyruvate dehydrogenase (PDH), leading to the depletion of acetyl coenzyme A, an important precursor in acetylcholine synthesis (R1)

References

1
Targeting Glycogen Synthase Kinase-3β for Therapeutic Benefit against Oxidative Stress in Alzheimer's Disease: Involvement of the Nrf2-ARE Pathway
2011