Given that tauopathy is a major outcome of ADNP deficiency or pathological ADNP mutations in mice [5, 17] and humans [10], and that NAP (davunetide) offered protection against tauopathy in multiple pre-clinical models [5, 17, 27], as well as provided indications of encouraging increased cognitive scores in an aMCI trial [15], progressive supranuclear palsy (PSP) was deemed to be an ideal target for davunetide-mediated protection. The gene discussed is ADNP; the disease is Classical progressive supranuclear palsy.