Open AccessBehavioral, 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
Author(s) -
Felipe Carmo de Moura,
Marluy Kildary Fernandes Xavier,
Francisca Eliane Lima Rodrigues,
Marcos Fabio dos Santos Pinheiro,
E Machado,
Caricia Bianca Carmo De Moura,
Wilson Max Almeida Monteiro de Moraes,
Jonato Prestes,
Edna Maria Camelo Chaves
Publication year - 2019
Publication title -
world scientific research
Language(s) - English
Resource type - Journals
eISSN - 2518-0177
pISSN - 2411-6661
DOI - 10.20448/journal.510.2019.61.5.13
Subject(s) - naltrexone , neurochemical , hippocampus , pharmacology , neuroprotection , donepezil , alzheimer's disease , medicine , psychology , endocrinology , antagonist , dementia , disease , receptor
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.