Abstract

Objective: Alzheimer’s disease (AD) is characterized by the production and deposition of amyloid-β peptide (Aβ) and neurofibrillary degeneration. It has been demonstrated that aluminum (Al) may be considered as a risk factor for developing the disease, while it is well established that Aβ induces oxidative stress, neurotoxicity and apoptosis. On the other hand, melatonin is a potent antioxidant whose levels are reduced in patients of AD in relation with the progression of the disease. Therefore, restoring the suitable melatonin levels could be considered a good strategy against AD. Materials and methods: The quantity of soluble and insoluble Aβ (Aβ1-40 and Aβ1-42, respectively), the main pro-apoptotic caspase (caspase-3), and the anti-apoptotic SOD2 protein levels in cortex and hippocampus of Tg2576 mice were evaluated. Animals were chronically exposed to Al and melatonin from diet and drinking water, respectively. Results: The quantity of Aβ40 was higher than the quantity of Aβ42 in brain tissues. However, no significant differences between groups were found. Regarding Casp-3 and SOD2, an interaction “genotype × treatment” was found in both tissues tested, but no significant differences between groups of treatment were noted. Conclusion: The results of the present study did not corroborate the anti-amyloidogenic and anti-apoptotic properties of melatonin. Further studies are required to confirm the tendencies here observed.


Author Details

Authors

• Celeste Di Paolo¹
• Jordi Blanco²
• Maria Cabré³
• Tania García^{1, 3}
• Mercedes Gómez^{1, 3}
• Jose L. Domingo¹

Departments

• ¹ Laboratory of Toxicology and Environmental Health,
• ² Physiology Unit, and
• ³ Biochemistry Unit, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Catalonia, Spain

Address

Professor Jose L. Domingo

Laboratory of Toxicology and Environmental Health
School of Medicine, IISPV, Universitat Rovira i Virgili
Reus, Catalonia, Spain

Email: [email protected]

Citation