Since SV2A is involved in the regulation of synaptic vesicle transport, exocytosis, and neurotransmitter release (Mendoza-Torreblanca et al., 2013), overexpression of SV2A may alleviate AD-related symptoms by reducing the content of Tau and thereby inhibiting the impairment of synaptic vesicle information transmission. The gene discussed is SV2A; the disease is Alzheimer disease.