Table of Contents:
  • The oligomer cascade hypothesis for Alzheimer's Disease
  • Why the oligomer hypothesis has largely supplanted the amyloid cascade hypothesis
  • The role of AβOs in memory failure and the major facets of AD neuropathology
  • Mechanisms by which AβOs instigate neurotoxicity
  • Why AβOs accumulate in the first place
  • How AβOs offer superb targets for novel AD diagnostics and disease-modifying therapeutics
  • Beside its direct link to Alzheimer's disease, the discovery of toxic Aβ oligomers has provided a novel structural archetype for toxins germane to more than two dozen diseases of protein mis-folding, including Diabetes, Parkinson's, and prion diseases