All these vascular dysfunctions might be due to a tau-induced dissociation of neuronal nitric oxide synthase (nNOS) and reduction of nitric oxide (NO) during glutamatergic synaptic activity, indicating the glutamatergic signaling dysfunction and NO deficiency as early signs of tau pathology and providing a possible mechanism for the neurovascular alterations in the prodromal phase of AD [58]. The gene discussed is MAPT; the disease is Alzheimer disease.