Abstract
Oxidative stress is a constant feature in the pathogenic mechanisms of Alzheimer's disease. Free radical overproduction derived from different pathways in those areas where amyloid-beta forms aggregate pushes the balance between endogenous antioxidants and the homeostatic redox control toward a state of oxidative stress. Additionally, a vicious cycle between oxidative stress and neuroinflammation is formed, which further complicates the return to a physiologic balance. Even though amyloid-beta, by itself, may initiate a free radical chain reaction, free radicals in the Alzheimer's brain come mainly from the microglial respiratory burst and from damaged mitochondria (electron leakage). The majority of Alzheimer hypotheses - including the cholinergic hypothesis, the mitochondrial cascade, the calcium hypothesis, the insulin resistance hypothesis and the lipid connection - all include oxidative stress-related processes. The amyloid-beta processing is itself an oxidative stress-related process. Melatonin is a free radical scavenger which additionally modulates the neuroinflammatory response and may even directly interact with the amyloid-beta, preventing its aggregation. This chapter is devoted to the antioxidant and anti-inflammatory role of melatonin in Alzheimer's neurodegeneration.
| Original language | English (US) |
|---|---|
| Title of host publication | Aging |
| Subtitle of host publication | Oxidative Stress and Dietary Antioxidants |
| Publisher | Elsevier Inc. |
| Pages | 177-193 |
| Number of pages | 17 |
| ISBN (Print) | 9780124059337 |
| DOIs | |
| State | Published - Mar 2014 |
Keywords
- Alzheimer's disease
- Antioxidants
- Free radical scavenger
- Melatonin
- Neurodegeneration
- Oxidative stress
ASJC Scopus subject areas
- Dentistry(all)
- Medicine(all)