Amyloid-β in Alzheimer's disease: The horse or the cart? Pathogenic or protective?

Hyoung Gon Lee, Rudy J. Castellani, Xiongwei Zhu, George Perry, Mark A. Smith*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

50 Scopus citations

Abstract

While the pathogenesis of Alzheimer's disease (AD) is unclear, amyloid-β plaques remain major lesions in the brain of individuals with AD. Likewise, amyloid-β is one of the best-studied proteins relating to the pathogenesis of AD. Indeed, the pathological diagnosis of AD tends to be congruous with the quantity of amyloid-β. However, it is important to recognize that pathological diagnosis merely represents the association of a pattern of pathological changes with a clinical phenotype. Therefore, it should be acknowledged that, although amyloid-β detection and semiquantification have some diagnostic utility, the simple presence of amyloid plaques, as with proteinaceous accumulations in essentially all neurodegenerative diseases, does not presume aetiology. Thus, in this review, we discuss the role of amyloid-β in the pathogenesis of AD and provide an alternative view to the widely accepted dogma.

Original languageEnglish (US)
Pages (from-to)133-138
Number of pages6
JournalInternational Journal of Experimental Pathology
Volume86
Issue number3
DOIs
StatePublished - Jun 2005
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Amyloid-β
  • Antioxidant
  • Oxidative stress
  • Senile plaque

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

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