But the CVN-AD model (APPSwDI +/+/mNos2-/-) also demonstrates metabolic impairment, intraneuronal tauopathy and phosphorylated tau, changes in neurovascular coupling, and severe neuronal degeneration and cognitive abnormalities, a process similar to AD, due to lack of mouse inflammatory nitric oxide synthetase (mNOS2) [3, 15, 16]. The gene discussed is MAPT; the disease is tauopathy.