ATG5 and prion disease: In prion disease model, SFN abolished neurotoxicity through inducing autophagy in human neuron cells exposed to prion protein (PrP) (106–126)-mediated neurotoxicity characterized by increased autophagy flux marker MAP1A/LC3II protein levels, and decreased p62 (an autophagy adaptor protein) levels via activating the AMPK pathway; this was, however, blocked by autophagy-related 5 (ATG5) protein knockdown [266].