Given that N-glycosylated AChE is significantly increased in the cerebrospinal fluid of patients with AD[12], and that the expression of AChE is negatively regulated by miR-132[65], which largely decreases in late-onset AD patients[66], it is plausible that the interaction between AChE and neurexin increases in the brains of AD patients, leading to damage at the glutamatergic synapses. The gene discussed is ACHE; the disease is Alzheimer disease.