Felipe Carmo De Moura
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Marluy Kildary Fernandes Xavier
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Francisca Eliane Lima Rodrigues
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Marcos Fabio dos Santos Pinheiro
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Erika Clemente Lima Machado
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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.
Behavioral, Neurochemical and Histological Changes in the Use of Low Doses of Naltrexone and Donepezil in the Treatment in Experimental Model of Alzheimer’s Disease by Induction of β-Amyloid1-42 in Rats