Insulin Resistance as a Link between Amyloid-Beta and Tau Pathologies in Alzheimer's Disease.

摘要: Current hypotheses and theories regarding the pathogenesis of AD heavily implicate brain IR as a key factor. Despite many well-validated metrics for systemic IR, absence biomarkers brain-specific represents translational gap that hindered its study in living humans. In our lab, we have been working to develop reflect common mechanisms may be used follow their engagement by experimental treatments. We present two promising AD: insulin cascade mediators probed extracellular vesicles (EVs) enriched neuronal origin, two-dimensional Magnetic Resonance Spectroscopy measures glucose. As further evidence fundamental link between AD, provide novel analysis demonstrating close spatial correlation expression genes implicated (using Allen Human Brain Atlas data) tau beta-amyloid pathologies. proceed propose bold baseline differences metabolic reliance glycolysis, glucose transporters signaling genes, determine vulnerability different regions Tau and/or Aβ pathology resistance is critical these pathologies define AD. Lastly, an overview ongoing clinical trials target angle treat suggest how evaluate treatment efficacy engagement.