In an ADNP-deficient mouse model (ADNP+/−), which presents with increased tau hyperphosphorylation, tauopathy-induced memory impairments, and neurodegeneration, 2 weeks of daily 0.5 μg IN-NAP to 2 and 9 month old mice partially ameliorated cognitive deficits and reduced tau hyperphosphorylation, showing that even short-term treatment can have significant effects on MCI/AD phenotypes at various stages of degeneration [105]. The gene discussed is ADNP; the disease is tauopathy.