Evaluación de los efectos de la exposición crónica a aluminio a través de la dieta en ratones Tg2576. Papel protector de la melatonina.

Identifier:  TDX:3313

Handle: https://hdl.handle.net/20.500.11797/TDX3313

Authors:  Di Paolo Pereyra, Celeste Gisela

Abstract:
Alzheimer's disease (AD) is a progressive, irreversible neurodegenerative disease with an unknowning origin. The hypothesis of the interaction of metals (and nowadays, in particular aluminum) with other factors to cause AD has been gaining importance through studies in which levels of different metals accumulated in the brains of AD patients (Cu, Fe, Zn, Al ...) were three to five times higher. The hypothesis of this study was: Melatonin is able to protect the brain from the biochemical and cognitive damages caused by chronic exposure to aluminum in a transgenic mouse model for Alzheimer's disease. For this purpose, learning and the memory have been evaluated, the concentrations of metals in different tissues have been measured and the concentration of caspase-3 and SOD2 present in cortex and hippocampus had been quantified. Finally, overexpression of the APP gene appears to generate an increase in activity. Treatment with AlCit causes learning deficits and inhibits long-term memory retention in Tg2576 mice. Melatonin does not appear to have any effect on the concentration of the metals studied. Also, there was no significant effect of melatonin treatment on the amount of Aβ in the cortex and hippocampus. The aluminum and citrate treated groups showed the highest levels of caspase-3 and SOD2 in both wild-type and Tg2576 groups and melatonin did not have a statistically significant protective effect.