Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 4, Issue 3, Pages 193-201Publisher
IOS PRESS
DOI: 10.3233/JAD-2002-4309
Keywords
-
Categories
Funding
- NIH [AG-05119, AG-10836, AG 14766]
- Zenith Award from the Alzheimer Association
- Alzheimer Forschung Initiative e.V. (AFI)
- Hirnliga
- SmithKlineBeecham-Stiftung
- Alexander-von-Humboldt Foundation
- Bundesministerium fur Bildung, Forschung und Technologie (BMB+F)
- Interdisziplinares Zentrum fur Klinische Forschung (IZKF) at the University of Leipzig [01KS9504]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available