Abstract
Advanced glycation endproducts (AGEs) accumulate on long-lived proteins, including β-amyloid plaques in Alzheimer's disease, and are suggested to contribute to neuronal dysfunction and cell death. We have investigated the effects of a model AGE upon glucose metabolism and energy production in a neuroblastoma cell line. AGEs decrease cellular ATP levels and increase glucose consumption and lactate production. All of the AGE-induced metabolic changes can be attenuated by antioxidants such as (R+)-α-lipoic acid and 17β-estradiol. These antioxidants may become useful drugs against (AGE-mediated) effects in neurodegeneration through their positive effects on cellular energy metabolism.
| Original language | English |
|---|---|
| Pages (from-to) | 1307-1313 |
| Number of pages | 7 |
| Journal | Journal of Cerebral Blood Flow and Metabolism |
| Volume | 23 |
| Issue number | 11 |
| DOIs | |
| Publication status | Published - Nov 2003 |
| Externally published | Yes |
Keywords
- Advanced glycation endproducts
- Antioxidants
- Lactate
- Lipoic acid
- Oxidative stress