Aluminium-induced electrophysiological, biochemical and cognitive modifications in the hippocampus of aging rats

Sethi, Pallavi; Jyoti, Amar; Singh, Rameshwar; Hussain, Ejaz; Sharma, Deepak

doi:10.1016/j.neuro.2008.08.005

Cited by 123 publications

(55 citation statements)

References 57 publications

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“…In addition, AlCl 3 -received group showed marked increase in the brain MAD associated with marked decrease in SOD and TAC as compared to control group indicating marked oxidative stress. These results are in accordance with the effect of Al exposure on the development of oxidative stress related damage to lipids, membrane associated proteins and endogenous antioxidant enzyme activity [47]. Results of the AlCl 3 -received group were also confirmed by the results of the histopathological examination of the brain in the present study which showed degeneration and pyknosis in hippocampus neurons, focal gliosis as well as focal eosinophilic plagues in the striatum in addition to congestion in blood vessels.…”

Section: Discussionsupporting

confidence: 90%

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

Ali¹,

Ahmed²

2016

J Alzheimers Dis Parkinsonism

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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 (AlCl 3 ) (70 mg/kg, IP) for AD mimic group, while treated groups received together with AlCl 3 , 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 AlCl 3 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 AlCl 3 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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Section: Discussionsupporting

confidence: 90%

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

Ali¹,

Ahmed²

2016

J Alzheimers Dis Parkinsonism

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“…Furthermore, Tsubouchi R et al reported that Al (mal) 3 induced apoptosis in PC12D cells by enhancing the generation of reactive oxygen species 2) . In contrast to the well-documented Al-induced cellular neurotoxicity, neurobehavioral studies of Al have generally not produced robust or consistent results 36,41) . Therefore, the potential toxicity of Al (mal) 3 requires further investigation.…”

Section: Discussionmentioning

confidence: 85%

“…If Al accumulation in the brain induces spatial memory impairment, it is conceivable that Al is one of the important factors impairing brain function and a potential contributing factor in the etiology and/or pathology of AD 23) . However, the exact mechanism of Al neurotoxicity in AD has not yet been reported 36) . Measurements of LTP may provide a sensitive index of the integrity of cognitive processes affected by Al exposure.…”

Section: Introductionmentioning

confidence: 99%

Aluminium-Maltolate-induced Impairment of Learning, Memory and Hippocampal Long-term Potentiation in Rats

Liang

Wang

et al. 2012

Ind Health

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Recently, aluminium (Al) has been proposed to be one of the environmental factors responsible for cause Alzheimer's disease (AD). However, the relationship between Al and AD is controversial. To investigate the effects of subchronic Aluminium-maltolate (Al (mal) 3 ) exposure on the behavioral, electrophysiological functions. Forty Sprague-Dawley (SD) rats were randomly distributed into five groups. Over two months, rats in the saline group received daily intraperitoneal (i.p.) injections 0.9% saline, rats in the maltolate group received 7.56 mg/kg maltolate, and rats in the 0.27, 0.54, 1.08 mg/kg Al (mal) 3 groups received i.p. administrations of these three doses, respectively. Neural behavior was assessed in Morris water maze. Long-term potentiation (LTP) in hippocampus was recorded. Al content in the neocortex was determined using a graphite furnace atomic absorption spectrophotometer. Our studies indicate that subchronic Al (mal) 3 exposure significantly impaired spatial learning and memory abilities, suppressed the LTP in the CA1 hippocampal area, and elevated Al levels in cerebral cortex in a dose-dependent fashion. In conclusion, low doses of Al (mal) 3 can still lead to dramatic Al accumulation in the brain, severely impair learning and memory capacities, and hippocampal LTP.

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“…Chronic exposure of animals to aluminum is associated with behavioural, neuropathological and neurochemical changes. Among them, deficits of learning and behavioural functions are most evident (Kummar et al, 2009;Ribes et al, 2010;Sethi et al, 2008). Also, when mice were injected with adjuvants containing aluminum in amounts equivalent to those given to US military service personnel, neuroinflammation and cell loss were found in spinal cord and motor cortex, together with memorial deficits (Petrik et al, 2007).…”

Section: Aluminum and Neurotoxicitymentioning

confidence: 99%

Alzheimer’s Disease and Metal Contamination: Aspects on Genotoxicity

Lima¹,

Vasconcellos²,

Montenegro³

et al. 2011

Alzheimer's Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets

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Aluminium-induced electrophysiological, biochemical and cognitive modifications in the hippocampus of aging rats

Cited by 123 publications

References 57 publications

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

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

Aluminium-Maltolate-induced Impairment of Learning, Memory and Hippocampal Long-term Potentiation in Rats

Alzheimer’s Disease and Metal Contamination: Aspects on Genotoxicity

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