Amyloid-β, tau alterations and mitochondrial dysfunction in Alzheimer disease: The chickens or the eggs?

Mark A. Smith, Kelly L. Drew, Akihiko Nunomura, Atsushi Takeda, Keisuke Hirai, Xiongwei Zhu, Craig S. Atwood, Arun K. Raina, Catherine A. Rottkamp, Lawrence M. Sayre, Robert P. Friedland, George Perry

Research output: Contribution to journalArticlepeer-review

63 Citations (Scopus)

Abstract

Alzheimer disease (AD) is defined pathologically and diagnostically defined by amyloid-β senile plaques and neurofibrillary tangles (NFT) composed of tau. From the time of their original description nearly a century ago, a major focus has been to understand the role that these lesions play in the pathogenesis of the disease. The majority favors the notion that these lesions cause the disease and therefore attempts at therapeutic intervention are focused on preventing lesions formation. However, this rationale may be misguided since new evidence from our laboratories and others suggest that the lesions not only occur as a by-product of the fundamental disease process but also that they may be protective.

Original languageEnglish
Pages (from-to)527-531
Number of pages5
JournalNeurochemistry International
Volume40
Issue number6
DOIs
Publication statusPublished - 2002

Keywords

  • Alzheimer disease
  • Amyloid antioxidant
  • Mitochondria
  • Neurofibrillary tangles
  • Oxidative stress
  • Senile plaques
  • Tau

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

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