Aluminium Induced Neurodegeneration in Rat Cerebrum in Presence of Ethanol Co-exposure

Introduction: Aluminium (AL) exposure leads to neurotoxicity and many problems in the body. AL role in Alzheimer's Disease (AD) is unknown and controversial to the scientists. According to World Health Organisation (WHO) provisional tolerable weekly intake of AL is 2 mg/kg body weight. Moderate intake of alcohol may favour body in coronary heart disease and diabetes mellitus, etc. Aluminium being cheaper along with increased consumption of alcohol, mixed with each other may induce neurotoxicity. Aim: The study was designed to identify the effects of AL in cerebrum of rats in presence of ethanol co-exposure. Materials and Methods: An experimental study was carried out at Dr. RP Government Medical College, Kangra and Government Medical College, Amritsar, India after due approval from the Institute Animal Ethics Committee. Thirty-two wistar rats were divided into one vehicle control and three experimental groups. Group I received the normal saline water as vehicle control group. Group II received AL chloride 4.2 mg/kg body weight as experimental group. Group III received ethanol 1 gm/kg body weight as experimental group. Group IV received both AL chloride 4.2 mg/kg body weight and ethanol 1 gm/kg body weight as experimental group. After treatment, brain cortex was processed for histopathological observation under microscope. Results: Cerebral cortex showed normal architecture of the brain with haematoxylin and eosin staining and cresyl violet staining and modified Bielchowsky silver staining in low and high magnification in vehicle control group. Experimental group treated with AL and ethanol separately showed reduction in the count of pyramidal cells with moderate neuronal degeneration with pyknotic nuclei. Vacuolar changes and pericellular spaces around the necrotic neurons were also seen. Combined AL and ethanol treated group showed acute neurodegeneration and necrosis of cortex indicating chromatolysis and loss of substances and Neurofibrillary Tangle (NFT) and plaque. Conclusion: It has been concluded that the ethanol induced the effects of AL on the cerebrum and plays a significant role in AD pathogenesis.