- Alzheimer’s disease, β-amyloid1-42, Naltrexone, Neurochemical, Behaviour, Histological changes.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that promotes the involvement of memory-related functions, characterized by the presence of amyloid plaques formed by the β-amyloid peptide (Aβ), and hyperphosphorylated Tau protein neurofibrillary tangles. Evidence suggests that the use of low doses of Naltrexone, an opioid antagonist, possibly promotes a modulation of the immune system and consequent neuroprotective effect. The present study uses the animal model of induction with β-amyloid1-42 (Aβ1-42) to verify the behavioral, neurochemical and histological effects of the use of low doses of Naltrexone. Male wistar rats (250-300g) divided into five groups (N = 8) were used: Control, Sham, Aβ1-42 subdivided into three groups: treated with water, 05 mg Donepezil and 4.5 mg Naltrexone, orally during the 30-day period. Behavioral tests demonstrated the efficacy of induction to the experimental model with reduced memory of Aβ1-42-treated animals as well as reversal of damage in animals treated with Naltrexone. In the structural analysis, observed that the animals induced by Aβ1-42 treated with water alone presented alterations in the pyramidal forms of the hippocampal cells and that the animals treated with Naltrexone presented possibly a reversal of the neuronal damages. In conclusion, treatment with Naltrexone promoted a reversal in the memory impairment of rodents induced to the Alzheimer's model with Aβ1-42 in the behavioral and histological response.