Alzheimercyclus: Rudolph Tanzi, Harvard University, USA

Title: The unifying role of innate immunity in the etiology and pathogenesis of Alzheimer's disease
Innate immune genes have been increasingly associated with AD. Most notably, we identified CD33 and TREM2, and elucidated there effects on microglial activation in AD. His groups has shown that aβ is an antimicrobial peptide (AMP), that is part of the brain’s innate immune system. It supports “The Antimicrobial Protection Hypothesis of AD”, which posits that AD neuropathology - beta- amyloid, NFT, and neuroinflammation - comprises an evolutionarily-conserved, orchestrated set of immune responses to protect the brain against infection. Furthermore, he posits that AD-associated genetic risk variants may be evolutionarily conserved based on their ability to bolster AD neuropathology as an innate immune defense.