Journal of Alzheimers Disease & Parkinsonism
Open Access

Research Article

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

Azza A Ali^1*, Hebatalla I Ahmed¹, Hanan A Abd El-Samea¹ and Ebtehal El-Demerdash²

¹Pharmacology and Toxicology Department, Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt

²Pharmacology and Toxicology Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt

*Corresponding Author:

Azza A Ali
Head of Pharmacology and Toxicology Department, Faculty of Pharmacy
Al -Azhar University, Cairo, Egypt
Tel: +20 01061905439
E-mail: azzamoro@gmail.com

Received date: May 03, 2016; Accepted date: May 09, 2016; Published date: May 16, 2016

Citation: Azza AA, Ahmed HI, El-Samea HAA, El-Demerdash E (2016) The Potential Effect of Caffeine and Nicotine Co-administration against Aluminuminduced Alzheimer’s disease in Rats. J Alzheimers Dis Parkinsonism 6:236. doi: 10.4172/2161-0460.1000236

Copyright: © 2016 Azza AA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized clinically by cognitive decline and memory loss. Caffeine and nicotine are the most commonly co-used psycho stimulants. Caffeine is one of the major contributors to the dietary antioxidants which prevent oxidative damage and may reduce the risk of chronic neurodegenerative diseases. Nicotine has the ability to decrease level of reactive oxygen species (ROS) in the hippocampus and suggested to attenuate the impairment of memory associated with AD. The study aimed to evaluate the influence of caffeine and nicotine co-administration against aluminium-induced neurotoxicity that mimics AD in rats. Five groups of rats were used and received daily for five weeks: Saline for control, aluminium chloride (AlCl3) (70 mg/kg, IP) for AD mimic group, while treated groups received together with AlCl3, either Caffeine (5mg/kg, IP), Nicotine (1 mg/kg, SC) or their combination. Three behavioral experiments were performed: Forced Swimming Test (FST), Morris Water Maze (MWM) task and Conditioned-Avoidance and Learning (CAL) test. Histo pathological changes in the brain and biochemical changes in Acetyl cholinesterase (AchE) as well as oxidative parameters; malon dialdehyde (MDA), superoxide dismutase (SOD), total anti oxidane capacity (TAC) were also evaluated for all groups. Results of the behavioral tests showed that caffeine and nicotine co-administration had more pronounced protecting effect from learning and memory impairment induced by AlCl3 than each one alone. Caffeine and nicotine co-administration also prevent neuronal degeneration in the hippocampus and the eosinophilic plagues in the striatum induced by AlCl3 while nicotine alone still showed mild gliosis in striatum. The marked protection of caffeine and nicotine co-administration confirmed also by the significant increase in TAC and SOD and decrease in MDA and AchE in brain tissue. In conclusion, co-administration of caffeine and nicotine can reduce the risk of neuronal degeneration in the hippocampus and attenuate the impairment of learning and memory associated with AD.

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