Nicotine and Parkinson's Disease: The Research

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1. Research at a Glance
2. The Papers
3. PubMed Topic Searches
4. More Nicotine Research
5. Connections
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Research at a Glance

What kind of study each paper on this page is, and when the papers were published. Hover over a bar for its count.

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The Papers (27)

Newest first. Study types on this page — Human trial: 2 · Human observational study: 1 · Review: 12 · Animal study: 10 · Cell study: 1 · Chemistry / laboratory method: 1. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Nicotine suppresses the neurotoxicity by MPP+/MPTP through activating α7nAChR/PI3K/Trx-1 and suppressing ER stress

Animal study, 2017. This study looked at whether nicotine protects nerve cells from MPP+ and MPTP, two toxins used in the lab to mimic Parkinson's disease damage, using rat-derived PC12 cells and mice. In the cells, nicotine reduced the toxin's damage, brought back a protective protein called thioredoxin-1, and lowered markers of cell stress; blocking the α7 nicotinic receptor or the PI3K signalling pathway cancelled these effects. In mice, giving nicotine beforehand improved movement and restored thioredoxin-1 and tyrosine hydroxylase, an enzyme needed to make dopamine, after MPTP exposure. These results come only from cells and mice, not people.

Cai Y, Zhang X, Zhou X et al. (2017). Nicotine suppresses the neurotoxicity by MPP+/MPTP through activating α7nAChR/PI3K/Trx-1 and suppressing ER stress. Neurotoxicology. — PubMed PMID: 28082123 · doi:10.1016/j.neuro.2017.01.002

Chronic nicotine treatment decreases LPS signaling through NF-κB and TLR-4 modulation in the hippocampus

Animal study, 2017. This study looked at whether giving nicotine daily for 14 days changes inflammation in the hippocampus, a memory area of the brain that has many nicotinic receptors, especially the alpha-7 type. The animals were then exposed to LPS, a piece of bacteria that triggers inflammation. In the animals given nicotine, LPS switched on less of NF-kB, an inflammation 'master switch', and less of the inflammation genes Tnf, Il1b, Nos2 and Tlr4. Drugs that block nicotinic receptors, including one that blocks only the alpha-7 type, cancelled this effect, which suggests nicotine acts through these receptors; the result comes from animals only, not from people.

Café-Mendes CC, Garay-Malpartida HM, Malta MB et al. (2017). Chronic nicotine treatment decreases LPS signaling through NF-κB and TLR-4 modulation in the hippocampus. Neurosci Lett. — PubMed PMID: 27984197 · doi:10.1016/j.neulet.2016.10.056

Activation of α7 nicotinic acetylcholine receptors protects astrocytes against oxidative stress-induced apoptosis: implications for Parkinson's disease

Animal study, 2015. This lab study tested whether nicotine protects astrocytes, the brain's support cells, which are linked to Parkinson's disease. In cells exposed to hydrogen peroxide, a source of oxidative stress, nicotine reduced astrocyte death and stopped the drop in a protective nerve-growth factor (GDNF). The protection disappeared when the alpha-7 nicotinic receptor was blocked, and it seemed to work by protecting the cells' mitochondria. In animals given the toxin MPTP to cause Parkinson's-like damage, nicotine eased symptoms, protected dopamine-making nerve cells, reduced the activation of immune cells in the brain and kept GDNF levels up, all through the same alpha-7 receptor. These results come only from cells and animals.

Liu Y, Zeng X, Hui Y et al. (2015). Activation of α7 nicotinic acetylcholine receptors protects astrocytes against oxidative stress-induced apoptosis: implications for Parkinson's disease. Neuropharmacology. — PubMed PMID: 25486621 · doi:10.1016/j.neuropharm.2014.11.028

The nicotinic cholinergic system function in the human brain

Review, 2015. This review looks at human brain-imaging studies of the nicotinic cholinergic system, the brain's network of nicotinic receptors. It covers research using functional MRI and PET scans in healthy people and in patients. The studies show mixed results: depending on the task, activity linked to this system sometimes went up and sometimes went down, in areas such as thinking, emotion and behavior. The authors suggest that these brain-activity patterns could help mark mental and brain disorders in which this system changes, such as addiction, Alzheimer's disease, Parkinson disease and schizophrenia, and could help in developing psychological and drug treatments.

Nees F (2015). The nicotinic cholinergic system function in the human brain. Neuropharmacology. — PubMed PMID: 25446570 · doi:10.1016/j.neuropharm.2014.10.021

Nicotine reduces established levodopa-induced dyskinesias in a monkey model of Parkinson's disease

Animal study, 2013. Researchers tested whether nicotine could reduce the involuntary movements, called dyskinesias, that levodopa can cause in Parkinson's disease. They used monkeys given a toxin to produce Parkinson-like symptoms and gave them nicotine in their drinking water. Some started nicotine after levodopa (23 monkeys) and some before it (26 monkeys); in both groups the involuntary movements fell by 60% to 70%, and the benefit lasted through the 17 to 23 weeks of the study. Nicotine did not make the Parkinson-like symptoms worse, but these results come from monkeys, not people.

Quik M, Mallela A, Ly J et al. (2013). Nicotine reduces established levodopa-induced dyskinesias in a monkey model of Parkinson's disease. Mov Disord. — PubMed PMID: 23836409 · doi:10.1002/mds.25594

A genetic basis for the variable effect of smoking/nicotine on Parkinson's disease

Human observational study, 2013. Smoking is known to be linked to a lower risk of Parkinson's disease. These researchers wanted to know whether a person's genes change that link, so they searched the whole genome in people and also in fruit flies exposed to nicotine and paraquat, a chemical that damages nerve cells. In people they found a gene called SV2C, which makes a protein in the tiny sacs that release dopamine in the part of the brain that Parkinson's damages. Depending on which version of SV2C a person carried, smoking's effect on Parkinson's risk ranged from protective to neutral to harmful. In the flies, nicotine and paraquat together changed the activity of a similar gene. The authors suggest SV2C may help explain who could benefit from nicotine in future studies, but the fly results are only in animals.

Hill-Burns EM, Singh N, Ganguly P et al. (2013). A genetic basis for the variable effect of smoking/nicotine on Parkinson's disease. Pharmacogenomics J. — PubMed PMID: 23032990 · doi:10.1038/tpj.2012.38

Is nicotine protective against Parkinson's disease? An experimental analysis

Animal study, 2012. This study used rats with damage to one side of the brain that mimics Parkinson's disease. The rats were given nicotine in their daily drinking water over a long period, to copy how smokers take in nicotine. Nicotine cut one drug-triggered movement problem (circling) by 40% but raised another by 230%, and it changed how dopamine receptors and certain brain cells behaved in the damaged area. The authors concluded that nicotine did not specifically protect brain cells from dying, but changed how the brain's dopamine system works, and suggested it might have a role in treating Parkinson's disease; these results are from rats only.

García-Montes JR, Boronat-García A, López-Colomé AM et al. (2012). Is nicotine protective against Parkinson's disease? An experimental analysis. CNS Neurol Disord Drug Targets. — PubMed PMID: 23131151 · doi:10.2174/1871527311201070897

Nicotine as a potential neuroprotective agent for Parkinson's disease

Review, 2012. This review looks at whether nicotine, and other drugs that act on the brain's nicotinic receptors, might help protect against Parkinson's disease. The idea began with population studies that linked smoking to fewer cases of Parkinson's disease. Later, giving nicotine protected the brain's dopamine pathway from damage in animal models of the disease. The authors describe how nicotine may work through several types of nicotinic receptors, calcium signalling, immune responses and growth factors. They also note that nicotine has antidepressant effects and improves attention and thinking, and they conclude that nicotine and related receptor drugs are promising treatments for Parkinson's disease.

Quik M, Perez XA, Bordia T (2012). Nicotine as a potential neuroprotective agent for Parkinson's disease. Mov Disord. — PubMed PMID: 22693036 · doi:10.1002/mds.25028

Can nicotine be used medicinally in Parkinson's disease?

Review, 2011. This review looks at whether nicotine could be used as a medicine for Parkinson's disease, starting from the observation that people who smoke have a lower risk of the disease. The authors report strong evidence from laboratory and animal studies that nicotine protects the dopamine-making nerve cells damaged in Parkinson's. In animal models, nicotine alone had slight or no effect on movement, but given with L-DOPA it reduced the involuntary movements (dyskinesias) that L-DOPA can cause. Clinical trials in people have so far been inconclusive, held back by different study designs and small numbers of patients, and there is still no agreement on the daily dose or how nicotine should be given.

Thiriez C, Villafane G, Grapin F et al. (2011). Can nicotine be used medicinally in Parkinson's disease?. Expert Rev Clin Pharmacol. — PubMed PMID: 22114853 · doi:10.1586/ecp.11.27

Nicotinic modulation of innate immune pathways via α7 nicotinic acetylcholine receptor

Review, 2010. This review looks at how nicotine affects the body's first-line immune defenses by acting on one type of nicotine receptor, called alpha-7, which is found on both nerve cells and immune cells. The authors summarize evidence that nicotine calms inflammation in several cell types and may help protect nerve cells in diseases linked to inflammation, such as Alzheimer's and Parkinson's disease. They note that nicotine has been tried in clinical trials for some inflammatory diseases, such as ulcerative colitis, but that how it works is still largely unknown. The authors say that understanding this mechanism may help in developing new medicines for infections and nerve-degenerating diseases.

Cui WY, Li MD (2010). Nicotinic modulation of innate immune pathways via α7 nicotinic acetylcholine receptor. J Neuroimmune Pharmacol. — PubMed PMID: 20387124 · doi:10.1007/s11481-010-9210-2

Nicotine binding to brain receptors requires a strong cation-pi interaction

Chemistry / laboratory method, 2009. This laboratory study looked at why nicotine attaches strongly to acetylcholine receptors in the brain but only weakly to the same type of receptor in muscle. At the alpha4beta2 brain receptor, which is thought to underlie nicotine addiction, nicotine's strong grip comes from a particular chemical attraction (a cation-pi interaction) with one amino acid of the receptor, called TrpB, and that attraction is mostly missing in the muscle receptor even though the binding sites are built from the same amino acids. A single small difference near TrpB seems to change the shape of the binding site, which lets nicotine bind more tightly in the brain receptor. The authors say these findings could help efforts to design drugs that act on specific types of nicotinic receptors, which are drug targets in conditions such as Alzheimer's disease, Parkinson's disease, schizophrenia, pain, depression and smoking cessation.

Xiu X, Puskar NL, Shanata JA et al. (2009). Nicotine binding to brain receptors requires a strong cation-pi interaction. Nature. — PubMed PMID: 19252481 · doi:10.1038/nature07768

Nicotine neuroprotection against nigrostriatal damage: importance of the animal model

Review, 2007. This review looks at whether nicotine can protect the brain cells lost in Parkinson's disease, a movement disorder. Tobacco users get Parkinson's disease less often, and in cell studies nicotine consistently protected nerve cells from damage. In animals the results were mixed: studies in mice disagreed with each other, while studies in rats and in monkeys with a condition much like human Parkinson's disease showed protection again and again. The authors conclude that choosing the right animal model and treatment conditions matters when testing possible brain-protecting treatments, and these findings come only from cells and animals, not from people.

Quik M, O'Neill M, Perez XA (2007). Nicotine neuroprotection against nigrostriatal damage: importance of the animal model. Trends Pharmacol Sci. — PubMed PMID: 17412429 · doi:10.1016/j.tips.2007.03.001

Application of nicotine enantiomers, derivatives and analogues in therapy of neurodegenerative disorders

Review, 2007. This review looks at how nicotine and closely related compounds have been studied as possible treatments for several brain and nervous-system conditions, including Alzheimer's disease, Parkinson's disease, Tourette's syndrome and schizophrenia. It also covers how nicotine is measured and extracted in the laboratory, how it acts on the body at the molecular level, and natural and synthetic nicotine-like compounds being considered for medical use. The authors compare the two mirror-image forms of nicotine found in nature and suggest that the less common form, (R)-nicotine, which they describe as less toxic, may have a place in medicine.

Pogocki D, Ruman T, Danilczuk M et al. (2007). Application of nicotine enantiomers, derivatives and analogues in therapy of neurodegenerative disorders. Eur J Pharmacol. — PubMed PMID: 17376429 · doi:10.1016/j.ejphar.2007.02.038

Nicotine induces brain CYP enzymes: relevance to Parkinson's disease

Review, 2006. This review looks at how nicotine affects certain liver-type enzymes (CYP2B6, CYP2D6 and CYP2E1) that are also found in the brain. Smokers have higher levels of these enzymes in the brain, and in animals nicotine raises their levels. These enzymes can break down several toxins that have been linked to Parkinson's disease. The authors suggest that this could help explain why smokers get Parkinson's disease less often, and they say it supports studying nicotine as a treatment to slow the disease. This is a proposed explanation that has not been tested in people.

Miksys S, Tyndale RF (2006). Nicotine induces brain CYP enzymes: relevance to Parkinson's disease. J Neural Transm Suppl. — PubMed PMID: 17017527 · doi:10.1007/978-3-211-45295-0_28

Chronic oral nicotine treatment protects against striatal degeneration in MPTP-treated primates

Animal study, 2006. Researchers gave monkeys nicotine in their drinking water for 6 months, which produced blood nicotine levels of 10 to 15 ng/mL, in the range seen in cigarette smokers. They then gave the monkeys low doses of MPTP, a toxin that damages the brain's dopamine system, over several months while the nicotine continued. Compared with monkeys that got the toxin but no nicotine, the nicotine-treated monkeys kept higher levels of several dopamine-related markers and of nicotinic receptors in the striatum, a brain area involved in movement. Nicotine had no effect in monkeys that did not get the toxin, and it did not prevent the loss of dopamine-producing cells in the substantia nigra. This was only in monkeys; the authors say the results support the possibility that nicotine contributes to the lower rate of Parkinson's disease seen in smokers.

Quik M, Parameswaran N, McCallum SE et al. (2006). Chronic oral nicotine treatment protects against striatal degeneration in MPTP-treated primates. J Neurochem. — PubMed PMID: 16882311 · doi:10.1111/j.1471-4159.2006.04078.x

Investigating the receptor-independent neuroprotective mechanisms of nicotine in mitochondria

Cell study, 2005. Nicotine has been linked to a lower risk of Parkinson disease, but no one knows why, so researchers tested it on mitochondria (the energy-producing parts of cells) taken from brains, and on human nerve-like cells grown in the lab. Nicotine reduced the swelling of mitochondria and the release of cytochrome c, a protein that signals a cell to die, when these were exposed to MPP+ (a nerve toxin) or calcium. It did not prevent the mitochondria from losing their electrical charge, but it did reduce electron leakage at a part of the energy chain called complex I. In the lab-grown cells, nicotine still delayed this damage from a mix of nerve toxins when a drug blocked nicotinic receptors, which suggests some of its protective effect does not depend on those receptors. These results come only from isolated mitochondria and cells, not from animals or people.

Xie YX, Bezard E, Zhao BL (2005). Investigating the receptor-independent neuroprotective mechanisms of nicotine in mitochondria. J Biol Chem. — PubMed PMID: 15985439 · doi:10.1074/jbc.M504664200

Nicotine and nicotinic receptor involvement in neuropsychiatric disorders

Review, 2004. This review looks at experimental and clinical research on nicotine and nicotinic receptors, the brain receptors that nicotine acts on, in several brain and mental health conditions. The authors say changes in the number or function of these receptors have been linked to Alzheimer's disease for several years. They describe growing evidence that the receptors may also play an important role in schizophrenia, Parkinson's disease, anxiety disorders and attention deficit-hyperactivity disorder (ADHD). The review aims to identify targets for developing new medicines.

Newhouse P, Singh A, Potter A (2004). Nicotine and nicotinic receptor involvement in neuropsychiatric disorders. Curr Top Med Chem. — PubMed PMID: 14754447 · doi:10.2174/1568026043451401

Poor tolerability of a transdermal nicotine treatment in Parkinson's disease

Human trial, 2003. This open study gave nicotine skin patches to 22 non-smoking people with well-controlled Parkinson's disease for 25 days, raising the dose in steps from 7 mg to 14 mg to 21 mg. Fourteen of the 22 (64%) had side effects such as nausea, vomiting and dizziness, and 10 of them dropped out of the study. Age, body weight, how long they had had the disease and how severe their movement problems were did not explain who tolerated it poorly. The authors note that similar nicotine doses were better tolerated in earlier studies and suspect that the way the skin patch releases nicotine may be a key factor.

Lemay S, Blanchet P, Chouinard S et al. (2003). Poor tolerability of a transdermal nicotine treatment in Parkinson's disease. Clin Neuropharmacol. — PubMed PMID: 14520160 · doi:10.1097/00002826-200309000-00004

Nicotine protects rat brain mitochondria against experimental injuries

Animal study, 2003. Researchers tested whether nicotine protects the energy-producing parts of brain cells (mitochondria) in rats, using two setups: brain mitochondria briefly deprived of oxygen and then re-oxygenated in the lab, and rats given the pesticide rotenone daily to cause a Parkinson-like condition. In the oxygen-deprivation test, mitochondrial breathing fell by 43.68% without nicotine and by 31.1% with nicotine. In the rotenone-treated rats, mitochondrial function dropped by 50.36% and harmful superoxide production rose by 56.03%, and long-term nicotine treatment limited all of this damage. These results come from rats and rat brain tissue only, and the authors suggest that one effect of nicotine may be to preserve mitochondrial function in the brain.

Cormier A, Morin C, Zini R et al. (2003). Nicotine protects rat brain mitochondria against experimental injuries. Neuropharmacology. — PubMed PMID: 12668050 · doi:10.1016/s0028-3908(03)00041-8

Transdermal nicotine in PD: a randomized, double-blind, placebo-controlled study

Human trial, 2001. This 12-week randomized, double-blind, placebo-controlled trial tested nicotine skin patches as an add-on treatment in 32 non-smoking people with Parkinson's disease. Patients wore either nicotine patches (17.5 mg of nicotine in the first week and 35.0 mg in the second and third weeks) or placebo patches that looked the same, followed by 3 weeks without patches. Movement, tremor, fine motor skill, walking speed, daily function and depression scores showed no significant difference between the nicotine and placebo groups. Side effects were mild and happened about as often in both groups, and the authors concluded that nicotine patches at this dose and treatment length did not help Parkinson's symptoms.

Vieregge A, Sieberer M, Jacobs H et al. (2001). Transdermal nicotine in PD: a randomized, double-blind, placebo-controlled study. Neurology. — PubMed PMID: 11571330 · doi:10.1212/wnl.57.6.1032

Nicotine prevents striatal dopamine loss produced by 6-hydroxydopamine lesion in the substantia nigra

Animal study, 2001. This study in rats tested whether nicotine could protect the brain's dopamine system from a toxin that damages the dopamine-producing area in the brain and is used to model Parkinson's disease. When nicotine (1 mg/kg, injected under the skin) was given 4 hours before a smaller toxin dose and again 20, 44 and 68 hours afterward, it significantly prevented the loss of dopamine in the striatum, a movement-control area of the brain. Nicotine given only before the toxin, or only afterward, did not prevent the loss, and it also did not protect against a larger toxin dose that wiped out almost all dopamine. A drug that blocks nicotinic receptors cancelled the protective effect, so the authors conclude that any protection in living animals depends on a repeated, intermittent dosing schedule and on how severe the brain damage is; these results are only in rats.

Costa G, Abin-Carriquiry JA, Dajas F (2001). Nicotine prevents striatal dopamine loss produced by 6-hydroxydopamine lesion in the substantia nigra. Brain Res. — PubMed PMID: 11150495 · doi:10.1016/s0006-8993(00)03087-0

Nicotine and brain disorders

Review, 2000. This review looks at the nicotinic receptors in the brain, the docking sites that nicotine acts on. It explains that these receptors matter for memory and thinking, and that they play a part in several brain disorders: Parkinson's disease, Alzheimer's disease, Tourette's syndrome, schizophrenia, depression and attention deficit disorder. The authors write that clinical studies of these same conditions found nicotine had beneficial effects, both as a treatment and as a way to help prevent them. It is a summary of earlier research, not a new study, and the abstract gives no patient numbers.

Mihailescu S, Drucker-Colín R (2000). Nicotine and brain disorders. Acta Pharmacol Sin. — PubMed PMID: 11263271

Nicotinic receptors and Parkinson's disease

Animal study, 2000. Researchers looked at nicotinic receptors, the docking sites that nicotine acts on, in monkeys and in nerve cells grown in a dish. In monkeys, the brain area that is damaged in Parkinson's disease made the building blocks for several types of these receptors, and some of them changed after a toxin damaged the dopamine-producing nerve pathway. In the dish, giving nicotine to dopamine nerve cells before a toxin that targets them protected the cells from damage. These results come only from animals and cells, and the authors suggest that drugs acting on nicotinic receptors may be useful for treating Parkinson's disease.

Quik M, Jeyarasasingam G (2000). Nicotinic receptors and Parkinson's disease. Eur J Pharmacol. — PubMed PMID: 10771017 · doi:10.1016/s0014-2999(99)00888-2

Nicotine prevents experimental parkinsonism in rodents and induces striatal increase of neurotrophic factors

Animal study, 1998. Researchers tested whether nicotine could protect the brain in mice and rats given chemicals that damage dopamine nerve cells and cause Parkinson's-like disease. Nicotine protected against this damage in both models, about as well as a comparison drug that blocks a different brain receptor (NMDA). Nicotine also raised two growth factors that support nerve cells (FGF-2 and BDNF) in the rat striatum, a brain area affected in Parkinson's disease, and a drug that blocks nicotinic receptors stopped the FGF-2 increase. The authors suggest that these growth factors may be one way nicotine protected the animals, but these results come only from rodents.

Maggio R, Riva M, Vaglini F et al. (1998). Nicotine prevents experimental parkinsonism in rodents and induces striatal increase of neurotrophic factors. J Neurochem. — PubMed PMID: 9832142 · doi:10.1046/j.1471-4159.1998.71062439.x

Does nicotine have beneficial effects in the treatment of certain diseases?

Review, 1996. This 1996 review looks at why smokers seem less likely to develop ulcerative colitis, Alzheimer's disease and Parkinson's disease, and suggests that nicotine itself may be responsible for this effect. The author explains that nicotine acts on nicotinic receptors in the brain, which are reduced in Alzheimer's and Parkinson's disease, and that these receptors also affect dopamine, a brain chemical involved in Parkinson's disease and Tourette's syndrome. The review says pure nicotine has no known cancer-causing properties and can be given through skin patches or tablets, but it also notes that nicotine has many harmful side effects and that no one should be encouraged to smoke. It concludes that nicotine may have some medical value, or at least may be useful for developing future drugs.

Birtwistle J, Hall K (1996). Does nicotine have beneficial effects in the treatment of certain diseases?. Br J Nurs. — PubMed PMID: 9006184 · doi:10.12968/bjon.1996.5.19.1195

Pharmacology of nicotine: addiction and therapeutics

Review, 1996. This review describes how nicotine works in the body, both as the substance that keeps people addicted to tobacco and as a medicine to help people quit smoking. Nicotine acts on nicotinic receptors in the nervous system, and its effects depend on how fast and by what route it is taken and on tolerance; a few people have been described who break down nicotine unusually slowly and make little cotinine. The authors note that nicotine affects most organ systems, but its contribution to smoking-related disease is still unclear. At the time, nicotine medicines were available as a gum, a skin patch and a nasal spray for quitting smoking, and nicotine was being studied for ulcerative colitis, Alzheimer's disease, Parkinson's disease, Tourette's syndrome, sleep apnea and attention deficit disorder.

Benowitz NL (1996). Pharmacology of nicotine: addiction and therapeutics. Annu Rev Pharmacol Toxicol. — PubMed PMID: 8725403 · doi:10.1146/annurev.pa.36.040196.003121

Beneficial effects of nicotine

Review, 1991. This 1991 review looks at what pure nicotine, apart from tobacco, does in the body. Nicotine attaches to nicotinic receptors throughout the body, which triggers the release of several brain chemical messengers, especially catecholamines and serotonin. The author lists possible effects of long-term use: reinforcing effects that can drive continued use, lower body weight, better performance, and possible protection against Parkinson's disease, Tourette's disease, Alzheimer's disease, ulcerative colitis and sleep apnea. The paper notes that nicotine in tobacco causes illness and death in millions of people, that these effects vary greatly in how reliable they are, and that this justifies further research into possible medical uses.

Jarvik ME (1991). Beneficial effects of nicotine. Br J Addict. — PubMed PMID: 1859921 · doi:10.1111/j.1360-0443.1991.tb01810.x

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PubMed Topic Searches

1. PubMed: Parkinson's Disease and nicotine (the search this page is built from)

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Connections

• Dopamine, Reward & How Habits Hijack You — interactive animation
• Nicotine: The Research
• Dr. Bryan Ardis on this subject — his claims, presented on their own pages and kept separate from this research collection
• The Nicotine Patch, animated
• Nicotinic Acetylcholine Receptors
• Cigarette Smoke — what burnt tobacco adds that nicotine alone does not
• Brain and Memory
• Mood and Mental Health
• Inflammation and Immunity
• Cancer Research
• Heart and Blood Vessels
• Metabolism and Weight
• Addiction and Withdrawal
• Patches, Gum and Delivery

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