Mechanistic studies establish RIPK1-driven necroptosis as clinically relevant in neurological pathologies: In Alzheimer’s disease models, pharmacological inhibition of RIPK1 by necrostatin-1 attenuates tau hyperphosphorylation and Aβ-induced neuroinflammation while rescuing cognitive impairment in APP/PS1 mice (Yang et al., 2017). This evidence concerns the gene RIPK1 and Cognitive impairment.