In this context, Soligo et al. demonstrated in STZ-induced diabetes does not deplete total brain NGF but skews its processing; mature NGF falls, whereas 34/50-kDa proNGF isoforms accumulate from week 4 onward, lowering the NGF/proNGF ratio and tracking the loss of TrkA- and ChAT-positive basal-forebrain cholinergic neurons, indicating defective maturation of NGF during the early progression of experimental diabetic encephalopathy [47]. This evidence concerns the gene CHAT and diabetic encephalopathy.