Abstract
In less than a decade, beginning with the demonstration by Floyd, Stadtman, Markesbery et al. [1] of increased reactive carbonyls in the brains of patients with Alzheimer's disease (AD), oxidative damage has been established as a feature of the disease. Here, we review the types of oxidative damage seen in AD, sites involved, possible origin, relationship to lesions, and compensatory changes, and we also consider other neurodegenerative diseases where oxidative stress has been implicated. Although much data remain to be collected, the broad spectrum of changes found in AD are only seen, albeit to a lesser extent, in normal aging with other neurodegenerative diseases showing distinct spectrums of change.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1475-1479 |
| Number of pages | 5 |
| Journal | Free Radical Biology and Medicine |
| Volume | 33 |
| Issue number | 11 |
| DOIs | |
| State | Published - Dec 1 2002 |
Funding
Work in the authors’ laboratories is supported by funding from the National Institutes of Health (NS38648, AG19356, AG14249) and the Alzheimer’s Association (IIRG-98-136, ZEN-99-1789, IIRG-00-2163-Stephanie B. Overstreet Scholars, IIRG-98-140, TLL-99-1872).
Keywords
- Alzheimer's disease
- Amyloid-β
- Antioxidants
- Free radicals
- Homeostasis
- Neurofibrillary tangles
- Oxidative stress
- Redox balance
- Senile plaque
- τ
ASJC Scopus subject areas
- Physiology (medical)
- Biochemistry