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

Abstract

Alzheimer disease (AD) is defined pathologically and diagnostically defined by amyloid-beta 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.

• Authors: 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
• Journal: Neurochemistry international (Neurochem Int) Vol. 40 Issue 6 Pg. 527-31 (May 2002) ISSN: 0197-0186 [Print] England
• PMID: 11850109 (Publication Type: Journal Article, Review)

Chemical References

• Amyloid beta-Peptides
• Apolipoproteins E
• tau Proteins

Topics

• Aging (metabolism)
• Alzheimer Disease (metabolism, pathology)
• Amyloid beta-Peptides (metabolism)
• Apolipoproteins E (metabolism)
• Humans
• Mitochondria (metabolism, pathology)
• Oxidative Stress (physiology)
• tau Proteins (metabolism)