"Nicotine improves attention in a wide variety of tasks in healthy volunteers. 2. Nicotine improves immediate and longer-term memory in healthy volunteers. 3. Nicotine improves attention in patients with probable Alzheimer's Disease," [Warburton D M, "Nicotine as a cognitive enhancer," Progress in Neuro-Psychopharmacology and Biological Psychiatry, 16(2): 181-91, Mar l992].
"In humans, nicotine-induced improvement of rapid information processing is particularly well documented.... Preliminary studies have found that some aspects of the cognitive deficit in Alzheimer's disease can be attenuated by nicotine." [Levin E D, "Nicotinic systems and cognitive function," Psychopharmacology, 108(4):417-31, l992]
"Despite the absence of change in memory functioning, these results demonstrate that DAT [Alzheimer's disease] patients have significant perceptual and visual attentional deficits which are improved by nicotine administration." [Jones G M, Sahakian B J, et al, "Effects of acute subcutaneous nicotine on attention, information processing and short-term memory in Alzheimer's disease," Psychopharmacology, 108(4):485-94, l992].
Researchers have long been aware that fewer smokers get Alzheimer's diseases than non-smokers. Up to April 1992, of the 17 studies on Alzheimer's and smoking which had been published in peer-reviewed journals, 13 reported a reduced risk for smokers and only four found no difference between smokers and non-smokers. Similar findings have been published on the effect of smoking and Parkinson's disease.
In an article in The Times of London (9/7/93), Dr. James Le Fanu provided an examination of the research on smoking and its apparent protective effect for certain diseases. Dr. Le Fanu stated unequivocally: "Smokers have a 50 per cent reduced risk of developing Alzheimer's--and the more smoked the greater the protection."
So striking was the apparent protective effect of smoking on Alzheimer's that increasingly biomedical researchers are experimenting with nicotine to treat the symptoms of these dread disease in-patients who have been diagnosed as having them. Results from these experiments have all showed promise in alleviating the symptoms of these diseases with the administration of nicotine.
The mechanism by which the nicotine in tobacco works to protect smokers is that it increases the number of so-called "nicotinic" receptors in the brain, which in turn influence the production and release of the neurotransmitter acetylcholine. Those who come down with Alzheimer's show a marked loss of "nicotinic" receptors in their brains and thus have reduced levels of acetylcholine, which is necessary for memory and other brain functions.
Research has shown that tobacco smoke (and the nicotine therein) inhibits the activity of monoamine oxidase B (MAOB). Experiments on mice which were genetically engineered to be without the gene for MAOB "were resistant to the neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease," (Dr. Jean C. Shih researcher at the University of Southern California, as reported in Reuters, 10/7/97, "Isoenzyme Inhibited by cigarette Smoke May Have Role in Aging and Neurodegeneration"). The findings of Dr. Shih and her colleagues point to a protective effect from smoking on the aging of the brain.
While the amount of the publications, pointing on the cigarette smoking positive effect on Alzheimer's Patients, has decreased recently, in proportion with the strong worldwide campaign against smokers, there are still here and there posted studies results, supporting this viewpoint.
Findings on cigarette smoking to delay the onset of Alzheimer's disease were presented in 2004 by the Proceedings of the National Academy of Sciences indicate that nornicotine, a by-product of nicotine, could be responsible for this protective effect. Kim Janda and Tobin Dickerson of the Scripps Research Institute tested the effect of nornicotine on amyloid beta proteins, which aggregate into the plaques that are a hallmark of Alzheimer's disease.
Specifically, the researchers found that a reaction known as glycation, which occurs between the molecule and sugars, alters amyloid proteins so that fewer plaques can form. The authors note that together with nicotine, nornicotine is an intriguing and potentially valuable treatment for Alzheimer's disease.
Team of neuroscientists at the University of South Florida College of Medicine presented in 2004 another evidence of an anti-inflammatory mechanism in the brain by which nicotine may protect against nerve cell death. Their study was published in the Journal of Neurochemistry. In laboratory experiments, the researchers demonstrated that nicotine inhibits activation of brain immune cells known as microglia. Chronic microglial activation is a sign of brain inflammation that is a key step in nerve cell death. The researchers also identified the specific site, the alpha-7 acetylcholine receptor subtype, to which nicotine binds to block microglial activation.
Specifically, the researchers found that a reaction known as glycation, which occurs between the molecule and sugars, alters amyloid proteins so that fewer plaques can form. The authors note that together with nicotine, nornicotine is an intriguing and potentially valuable treatment for Alzheimer's disease.
Team of neuroscientists at the University of South Florida College of Medicine presented in 2004 another evidence of an anti-inflammatory mechanism in the brain by which nicotine may protect against nerve cell death. Their study was published in the Journal of Neurochemistry. In laboratory experiments, the researchers demonstrated that nicotine inhibits activation of brain immune cells known as microglia. Chronic microglial activation is a sign of brain inflammation that is a key step in nerve cell death. The researchers also identified the specific site, the alpha-7 acetylcholine receptor subtype, to which nicotine binds to block microglial activation.
Nicotine mimics the neurotransmitter acetylcholine, a chemical messenger that is critical to communication between brain cells. Acetylcholine is the major neurotransmitter lost in Alzheimer's disease. The prevailing hypothesis among researchers is that nicotine helps protect the brain by binding to nicotinic acetylcholine receptors that sit on the end of nerve terminals. This action by nicotine, similar to turning up the volume of a radio signal, causes brain cells to increase the release of neurotransmitters depleted in diseases like Alzheimer's.
Concluding this post, I would like to admit, that there are multiple research papers, claiming that tobacco smoking can be considered as a risk factor for Alzheimer's Disease, and it affects negatively the health and well-being of the AD patients. The post does not include these studies, and they will be reviewed in one of the future articles.
The controversy is based on the complexity of the tobacco ingredients, so looking in different components might lead to the opposite results. Taking in an account the overall health danger from smoking, we do not encourage you to pick up this habit, if you never smoked before. But, it is always good to see both sides of the story…
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