The phenotype of tau pathology in the full-length TauΔK described above was relatively mild, correlating with a low expression of exogenous mutant TauΔK (~two-fold overexpression of hTau40 over mTau) [11], a moderate propensity for forming β-structured tau amyloid fibrils, and a late onset of cognitive decline (~12 months). The gene discussed is MAPT; the disease is Mental deterioration.