Therefore, abundant levels of β-sheet rich PrPSc, decreased TRADD and TRAF2 level, and increased RIPK1, caspase-8 level along with sustained FADD expression might activate p75NTR either independently or in complex with DR6 to trigger neuronal damage over neuroprotection, highlighting its multifaceted role in pathophysiological mechanism in this mouse prion disease model. This evidence concerns the gene FADD and prion disease.