Journal
JOURNAL OF PINEAL RESEARCH
Volume 45, Issue 4, Pages 497-505Publisher
WILEY
DOI: 10.1111/j.1600-079X.2008.00626.x
Keywords
aging; amyloid beta; brain; cysteine proteases; sirt1
Categories
Funding
- Spain's Ministerio de Educacion y Ciencia [SAF2005-01604, SAF2006-13092]
- Instituto de Salud Carlos III [FISS-06-RD06/0013/0011]
- Autonomous Government of Catalonia [2005/SGR00893, TV3 (063230)]
Ask authors/readers for more resources
We examined the effect of melatonin on pro-survival processes in three groups of mice. Untreated senescence-accelerated mice (SAMP8), melatonin-treated SAMP8 and untreated senescence-accelerated resistant mice (SAMR1) of 10 months old were studied. Melatonin (10 mg/kg) or vehicle (ethanol at 0.066%) was supplied in the drinking water from the end of the first month until the end of the ninth month of life. Differences in the Akt/Erk1-2 pathway and downstream targets were examined and no significant changes were observed, except for beta-catenin. However, sirtuin 1 expression was significantly lower in SAMP8 than in SAMR1. In addition, acetylated p53 and NF kappa B expression were lower in SAMP8 than in SAMR1. These changes were prevented by melatonin. Moreover, the concentration/expression of alpha-secretase was lower and that of amyloid beta aggregates (A beta) was higher in untreated SAMP8 than in SAMR1. Likewise, the levels of Bid were higher, whereas Bcl-2(XL) levels were lower in SAMP8 than in SAMR1. Melatonin reduced all these changes. We conclude that melatonin improves pro-survival signals and reduces pro-death signals in age-related impairments of neural processes.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available