Raj et al.: Evaluation of Brain Training Effects on Cigarette Smoke Induced Dementia: An In vivo Study Alzheimer's disease is a chronic neurodegenerative disease among the elderly population. Various genetic, environmental and lifestyle factors have been associated with the etiology of Alzheimer's disease. Cigarette smoke has been reported to be a major predisposing factor for Alzheimer's disease and contributes to disease development. Conversely, studies have reported beneficial effects of brain training on the disease condition. The purpose of this study was to evaluate the effect of a brain training task in cigarette smoke induced dementia. Three groups of female C57 black 6 mice were used in the study with two of the groups subjected to cigarette smoke exposure. The third group was subjected to a novel object test immediately after the exposure. Brain training improved the cognitive domains of the smoke exposed mice. Brain training could also regain the neurotransmitter imbalances induced by cigarette smoke, importantly, decreased the glutamate levels in the hippocampus. Brain training also significantly decreased the hippocampal amyloid precursor protein expression levels by reducing the reactive oxygen species production. Additionally, the improved hippocampal neuronal count, post training supported the findings. The results indicated that brain training significantly decreased the deleterious effects of cigarette smoke in hippocampus tissue and improved dementia symptoms.

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Dementia is defined by the debilitation of cognition and behavior of individuals more than 65 y. Alzheimer's disease (AD) is the most pervasive pervasive form of dementia, afflicting around 47 million individuals worldwide. Oxidative damage is a significant component in the pathophysiology of Alzheimer's disease (AD). Assessment of Alzheimer's disease mind has shown a lot of oxidative harm, related with both trademark pathologies (senile plaques and neurofibrillary tangles) just as in typical seeming pyramidal neurons. By the by, the process that eventually causes disruption of redox balance and furthermore the origin of the free radicals are as yet hazy. There is likewise the accessibility of proof that oxidative stress may enhance the conglomeration and production of Aβ and furthermore help the polymerization just as phosphorylation of tau, subsequently making a pernicious cycle that invigorates the development and even commencement of Alzheimer's. These neurotic trademarks have complex proportional collaborations with cholinergic abrasions. This review may give complemental data for understanding the relationship between oxidative stress, amyloid plaques, tau proteins and cholinergic system in processing of AD.