The model also has strong face validity as it replicates many of the core clinical (hypokinesia, oculomotor deficits, impaired survival), pathological (neurodegeneration, neuroinflammation, synapse loss) and biochemical (Tau hyperphosphorylation, mislocalization, misfolding, truncation, insolubility, and oligomerization) features of PSP. This evidence concerns the gene MAPT and supranuclear palsy, progressive, 1.