It protected both neuronal and vascular brain cells from Aβ insults, preserved synapses and reduced excessive tau protein phosphorylation, while at the same time reduced soluble endogenously produced Aβ peptides, diminished the signs of neuroinflammation and gliosis and alleviated cognitive deficits in different memory paradigms in AD animal models. The gene discussed is MAPT; the disease is Alzheimer disease.