Further evidence in support of a new amyloid-independent hypothesis for the pathogenesis of Alzheimer's disease is provided, with an expanded set of Alzheimer-causing mutations in the protease that produces amyloid.
NPRL2 gene therapy induces robust antitumor immunity and overcome anti-PD1 resistance through augmenting antigen-presentation and cytotoxic T cells activation in KRAS/STK11 mutant NSCLC in humanized mouse model.