Nicotine has long been held to possess procognitive properties.
Overshadowed by its addictive properties, this hypothesis has not been universal, and several scholars have challenged its very basics claiming that nicotine not only does not alleviate cognitive impairment but also exacerbates it.
Nevertheless, an accumulating mass of evidence emerging from both in vitro and in vivo studies has shown that nicotine or its metabolites protect brain cells and enhance working memory, executive function, and cognitive performance via increasing cholinergic tone as well as neurotrophic factors levels, and decreasing apoptosis, oxidative stress, excitotoxicity, and neuroinflammation.
For example, nicotine administration in patients with neurodegenerative disorders such as Alzheimer’s disease (AD) and mild cognitive impairment (MCI) has been presented as effective in relieving memory and learning impairments. This could be accomplished by nicotine-mediated alleviation of cell death by the aforementioned mechanisms. Of late, nicotine biotransformation products such as cotinine have been found to possess procognitive properties and be devoid of nicotinic addictive attributes.
The scope of this research topic encompasses but is not limited to the exploration of the alleged cognitive impacts of nicotine and its derivatives on the brain and cognitive outcomes in diseased or aging conditions.
We would also like to receive a broad range of submissions of experimental or clinical studies covering:
• The kinetics and dynamics of nicotine and its biotransformed metabolites in the brain;
• The effects of these agents on cognition-related molecular and cellular mechanisms;
• The impacts of these molecules on the cognitive behaviors of both animals and human beings;
• Their possible addictive or toxic effects.
Nicotine has long been held to possess procognitive properties.
Overshadowed by its addictive properties, this hypothesis has not been universal, and several scholars have challenged its very basics claiming that nicotine not only does not alleviate cognitive impairment but also exacerbates it.
Nevertheless, an accumulating mass of evidence emerging from both in vitro and in vivo studies has shown that nicotine or its metabolites protect brain cells and enhance working memory, executive function, and cognitive performance via increasing cholinergic tone as well as neurotrophic factors levels, and decreasing apoptosis, oxidative stress, excitotoxicity, and neuroinflammation.
For example, nicotine administration in patients with neurodegenerative disorders such as Alzheimer’s disease (AD) and mild cognitive impairment (MCI) has been presented as effective in relieving memory and learning impairments. This could be accomplished by nicotine-mediated alleviation of cell death by the aforementioned mechanisms. Of late, nicotine biotransformation products such as cotinine have been found to possess procognitive properties and be devoid of nicotinic addictive attributes.
The scope of this research topic encompasses but is not limited to the exploration of the alleged cognitive impacts of nicotine and its derivatives on the brain and cognitive outcomes in diseased or aging conditions.
We would also like to receive a broad range of submissions of experimental or clinical studies covering:
• The kinetics and dynamics of nicotine and its biotransformed metabolites in the brain;
• The effects of these agents on cognition-related molecular and cellular mechanisms;
• The impacts of these molecules on the cognitive behaviors of both animals and human beings;
• Their possible addictive or toxic effects.
