The premature suspension of the amyloid- vaccine for the treatment of Alzheimer disease (AD), while disappointing, is not surprising. Amyloid- serves a key role in redox homeostasis (Nunomura et al., 2001) and its removal, by vaccination (or others) strategies, would be predicted to increase oxida
Alzheimer vaccine: amyloid-β on trial
✍ Scribed by Stephen R. Robinson; Glenda M. Bishop; Gerald Münch
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 106 KB
- Volume
- 25
- Category
- Article
- ISSN
- 0265-9247
No coin nor oath required. For personal study only.
✦ Synopsis
A new therapeutic approach is being developed for the treatment of Alzheimer's disease (AD). This approach involves the deliberate induction of an autoimmune response to amyloid-beta (Abeta) peptide, the constituent of neuritic plaques that is thought to cause the neurodegeneration and dementia in AD. If this approach is to be effective, antibodies must be produced that can selectively target the toxic forms of Abeta, while leaving the functionally-relevant forms of Abeta and its precursor protein untouched. Furthermore, an approach needs to be found that avoids provoking an acute neuroinflammatory response. The situation is made even more challenging by uncertainty regarding which isoforms of Abeta contribute to the pathogenesis of AD.
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