4.5 Article

Amyloid beta-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain exists

Journal

JOURNAL OF ALZHEIMERS DISEASE
Volume 4, Issue 3, Pages 193-201

Publisher

IOS PRESS
DOI: 10.3233/JAD-2002-4309

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Funding

  1. NIH [AG-05119, AG-10836, AG 14766]
  2. Zenith Award from the Alzheimer Association
  3. Alzheimer Forschung Initiative e.V. (AFI)
  4. Hirnliga
  5. SmithKlineBeecham-Stiftung
  6. Alexander-von-Humboldt Foundation
  7. Bundesministerium fur Bildung, Forschung und Technologie (BMB+F)
  8. Interdisziplinares Zentrum fur Klinische Forschung (IZKF) at the University of Leipzig [01KS9504]

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Alzheimer's disease (AD) brain is characterized by excess deposition of amyloid beta-peptide (A beta), particularly the 42-amino acid peptide [A beta(1-42)] and by extensive oxidative stress. Several sources of the oxidative stress and inflammatory cascades are likely, including that induced by advanced glycation end products, microglial activation, and by A beta(1-42) and its sequelae. This review briefly examines each of these sources of oxidative stress and inflammation in AD brain and discusses their potential roles in the clinical progression of AD dementia.

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