The amyloid-β peptide: Guilty as charged?

M. Paul Murphy, Valeria A. Buzinova, Carrie E. Johnson

Research output: Contribution to journalArticlepeer-review


Recent years have seen both considerable progress and controversy in the Alzheimer's disease (AD) field. After decades of slow to negligible movement towards the development of disease modifying therapies, promising outcomes in recent clinical trials with several monoclonal antibodies targeting various forms of the amyloid-β (Aβ) peptide have at last opened a possible way forward. In fact, at this point multiple anti-Aβ therapeutics are close to receiving (or have already received) regulatory approval. Although these outcomes are not without some degree of divisiveness, the fact remains that targeting amyloid for removal has finally shown at least modest efficacy in slowing the otherwise relentless progression of the disease. Although the validation of the long standing amyloid cascade hypothesis would seem to be at hand, what remains is the puzzling issue of why – if Aβ indeed causes AD – does removing it from the brain not stop the disease entirely.

Original languageEnglish
Article number166945
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Issue number2
StatePublished - Feb 2024

Bibliographical note

Publisher Copyright:
© 2023 Elsevier B.V.


  • APP
  • Amyloid
  • Fibril
  • Oligomer
  • Plaques
  • β-Amyloid precursor protein

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology


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