The Beta Amyloid Dysfunction (BAD) Hypothesis for Alzheimer’s Disease

@AdrianoAguzzi https://t.co/4pJwB5NRFN BAD hypothesis, of course based on data.

@tanyalewis314 @sciam Original cascade hypothesis is wrong. It does not assess a physiological role for normal non misfolded Abeta monomer. Since clinical Abeta compounds except Aducanumab, involved Abeta monomer, they had to fail. A new Abeta hypothes

@abcnews Except Aducanumab all clinical Abeta treatments were directed towards lowering Abeta production or Abeta monomer neutralization. Giving Abeta monomer a physiological function will explain all negative results and guide us to promising Abeta oligom

@realJacobBell @ByJonGardner The difference between all unsuccessful Abeta targeting drugs, like solanezumab and ganterumab including all BACE and Gamma secretase and the successful ones, like Aducanumab and BAN2401 is the cross reaction with essential na