| First Author | Quinn J | Year | 2005 |
| Journal | Brain Res | Volume | 1037 |
| Issue | 1-2 | Pages | 209-13 |
| PubMed ID | 15777772 | Mgi Jnum | J:97479 |
| Mgi Id | MGI:3575496 | Doi | 10.1016/j.brainres.2005.01.023 |
| Citation | Quinn J, et al. (2005) Chronic melatonin therapy fails to alter amyloid burden or oxidative damage in old Tg2576 mice: implications for clinical trials. Brain Res 1037(1-2):209-13 |
| abstractText | Melatonin has been proposed as a treatment for Alzheimer's disease based on the demonstration of antioxidant and 'anti-amyloid' effects in vitro and in vivo. Chronic melatonin therapy in old, amyloid plaque-bearing transgenic mice was studied. Tg2576 mice started melatonin treatment at 14 months of age. After 4 months of treatment, there were no differences between untreated and melatonin-treated mice in cortical levels of soluble, formic acid extracted, or histologically detectable beta amyloid (Abeta), nor in brain levels of lipid peroxidation product (total 8,12-isoprostane F(2alpha)-VI), despite marked elevations in plasma melatonin. We conclude that melatonin fails to produce anti-amyloid or antioxidant effects when initiated after the age of amyloid plaque deposition. These findings diminish the possibility that melatonin will be useful for the treatment of established Alzheimer's disease. |
