Anabolic Androgenic Steroid predisposes to the neuropathology of Alzheimer’s disease: insights from Animal model

Abstract

AbstractBackgroundAnabolic androgenic steroids (AASs) are synthetic derivatives of testosterone use for body enhancement by athletes and its use has been abused over the years. Various studies have reported the harmful potential of AAS use, however, there is need to document its possibility as a risk factor in neuropathology of dementia. This study is to demonstrate potential of AAS as a risk factor in Alzheimer’s disease (AD) pathology by demonstrating changes in the neuro‐morphology, astrocytic proliferation and neurofibrillary tangle formation in animal model.MethodTwenty (20) adult male Wistar rats used were divided into four groups (A‐D), treated as follows, Control (A), Olive oil as vehicle (B), oral 120mg/kg of AAS for 21days (C), and 7 days withdrawal group following 120mg/kg/ 21days of AAS intake (D). Serum was assayed for lipid peroxidation marker Malondialdehyde (MDA) and antioxidant enzyme ‐superoxide Dismutase (SOD). The prefrontal cortices were processed and stained for Nissl (chromatophilic) bodies, astrocytes immunohistochemistry and Bielschowsky stain for neurofibrillary tangles.ResultAAS treated group has characteristic pathology of AD demonstrated by the presence of necrosis, chromatolysis, marked astrocytic proliferation and presence of neurofibrillary tangles using Bielschowsky stain along with an increase in MDA and decline in endogenous SOD activities as compared with the control and olive oil treated groups. The withdrawal group (D) had a notable or mild restoration of the neurons demonstrated by presence of few necrotic neurons, reduced reactive astrocytes (astrogliosis) proliferation, decline in MDA with an increase in SOD when compared to the AAS treated group.ConclusionAAS has the potential to predispose individual to the neuropathology of AD characterized by neurodegeneration, astrogliosis, neurofibrillary tangles even in the presence of endogenous antioxidant enzyme, however, upon discontinuation endogenous antioxidant enzyme level increases enabling neuro repair via mobbing off free radicals generated by AAS.