Abstract
Alzheimer's disease (AD) brain is characterized by excess deposition of amyloid β-peptide (Aβ), particularly the 42-amino acid peptide [Aβ(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 Aβ(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.
| Original language | English |
|---|---|
| Pages (from-to) | 193-201 |
| Number of pages | 9 |
| Journal | Journal of Alzheimer's Disease |
| Volume | 4 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Jun 2002 |
| Externally published | Yes |
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