Choline acetyltransferase (ChAT) and AChE enzymes control ACh synthesis and breakdown10. The defect in ChAT activity or hyperactivity of AChE in AD patients prompts a considered reduction in ACh content at the synaptic cleft in the cortex, hippocampus, and amygdala. Thus, repairing cholinergic neuronal malformations is a target for improving cognitive disorders in AD patients. The gene discussed is CHAT; the disease is Alzheimer disease.