Nicotine and Alzheimer'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
6. Featured Videos

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 (30)

Newest first. Study types on this page — Review: 17 · Animal study: 6 · Cell study: 5 · Chemistry / laboratory method: 2. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Age- and Nicotine-Associated Gene Expression Changes in the Hippocampus of APP/PS1 Mice

Animal study, 2019. This study used mice bred to develop Alzheimer's-like brain changes. Researchers compared gene activity in the hippocampus, a memory area of the brain, in 18-month-old and 7-month-old mice, and also looked at how nicotine treatment changed gene activity at each age. The older mice had higher activity in genes linked to calcium overload, immune response and nerve-cell connections, including 14 types of calcium channel, and lower activity in genes linked to energy production and metabolism. Nicotine changed different genes at different ages: in young mice it increased fat-related metabolism and reduced certain cell-signaling pathways, while in old mice it affected genes tied to cell aging and death, and the authors suggest that extra nicotinic stimulation might not help in late-stage disease. These results come from mice only.

Yang J, Long Y, Xu DM et al. (2019). Age- and Nicotine-Associated Gene Expression Changes in the Hippocampus of APP/PS1 Mice. J Mol Neurosci. — PubMed PMID: 31399937 · doi:10.1007/s12031-019-01389-7

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

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

Stress and the α7 nicotinic acetylcholine receptor

Review, 2012. This review looks at how nicotine interacts with the body's stress system in people and laboratory animals. It says nicotine is well known to harm health, but it also notes research suggesting nicotine can help thinking and memory and may have a protective or easing role in Alzheimer's disease and schizophrenia. The authors focus on one nicotine receptor, the alpha-7 nicotinic receptor, which they describe as a key link between nicotine, the stress system and these diseases. They also report that this receptor has been shown to protect brain cells through several pathways, which makes it a reasonable target for developing treatments for a number of brain disorders.

Hunter RG (2012). Stress and the α7 nicotinic acetylcholine receptor. Curr Drug Targets. — PubMed PMID: 22300027 · doi:10.2174/138945012800398982

Neuroprotection by nicotine against colchicine-induced apoptosis is mediated by PI3-kinase--Akt pathways

Cell study, 2012. Researchers grew brain nerve cells from the cortex in the laboratory and damaged them with colchicine, a drug that disrupts the cell's internal scaffolding and can make nerve cells self-destruct. Nicotine protected the cells from this damage. The protection disappeared when the researchers blocked the alpha-7 nicotinic receptor or a survival signalling pathway called PI3K-Akt, so the authors conclude that the effect works through these two. The results come only from cells in a dish, not from animals or people.

Huang X, Cheng Z, Su Q et al. (2012). Neuroprotection by nicotine against colchicine-induced apoptosis is mediated by PI3-kinase--Akt pathways. Int J Neurosci. — PubMed PMID: 22248034 · doi:10.3109/00207454.2012.657377

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

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

Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease

Animal study, 2005. Researchers gave nicotine in the drinking water over a long period to mice bred to develop both of the main brain changes seen in Alzheimer's disease: amyloid plaques and tangles of a protein called tau. Long-term nicotine increased the number of nicotinic receptors in the brain, and this went along with a marked increase in tau clumping and in a chemical change to tau (phosphorylation) that is linked to tangles, so nicotine made the tau damage worse in these mice. The authors trace the tau change to the activation of an enzyme called p38 MAP kinase, and they also found that these Alzheimer's-model mice lose a type of nicotinic receptor (alpha7) from 6 months of age in the brain regions where amyloid builds up inside nerve cells. These results come from mice only.

Oddo S, Caccamo A, Green KN et al. (2005). Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease. Proc Natl Acad Sci U S A. — PubMed PMID: 15705720 · doi:10.1073/pnas.0408500102

Nicotine attenuates beta-amyloid peptide-induced neurotoxicity, free radical and calcium accumulation in hippocampal neuronal cultures

Cell study, 2004. Researchers grew brain nerve cells from the hippocampus, a memory area, in the laboratory and exposed them to beta-amyloid, the protein that builds up in the brain in Alzheimer's disease. Nicotine protected these cells from beta-amyloid-induced cell death, reduced the activity of cell-death enzymes, and lowered the buildup of harmful free radicals and calcium inside the cells. When a drug that blocks nicotinic receptors was added, part of this protection was lost, which suggests the effect works partly through these receptors. These results come only from cells in a dish; the authors suggest nicotine may help slow diseases such as Alzheimer's, but this was not tested in animals or people.

Liu Q, Zhao B (2004). Nicotine attenuates beta-amyloid peptide-induced neurotoxicity, free radical and calcium accumulation in hippocampal neuronal cultures. Br J Pharmacol. — PubMed PMID: 14757701 · doi:10.1038/sj.bjp.0705653

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

Nicotinic receptors in aging and dementia

Review, 2002. This review looks at research on nicotinic receptors, the brain receptors that nicotine acts on, in aging and dementia. The authors report that nicotine and similar compounds have improved thinking and memory in older or impaired subjects. They also report that some population studies link smoking to lower rates of neurodegenerative disease, and that nicotine protected nerve cells in animal and cell studies. Brains with dementia often lose this receptor system, and the authors suggest that drugs acting on these receptors might slow these diseases or improve function, but this is a hypothesis they put forward for discussion, not a tested result.

Picciotto MR, Zoli M (2002). Nicotinic receptors in aging and dementia. J Neurobiol. — PubMed PMID: 12436427 · doi:10.1002/neu.10102

Nicotinic receptor subtypes and cognitive function

Review, 2002. This review looks at how nicotinic receptors in the brain, the receptors nicotine acts on, are involved in thinking and memory. It notes that nicotine has been shown to improve attention in people with Alzheimer's disease, schizophrenia and ADHD, and that new drugs acting on specific receptor subtypes might work better with fewer side effects. In the authors' own experiments, which were done only in rats, both short-term and long-term nicotine improved working memory in a maze. Blocking either of two receptor types (alpha4beta2 or alpha7) in two brain areas, the hippocampus and the amygdala, impaired working memory, and long-term nicotine reversed the impairment caused by blocking alpha4beta2 in the hippocampus but not the impairment caused by blocking alpha7.

Levin ED (2002). Nicotinic receptor subtypes and cognitive function. J Neurobiol. — PubMed PMID: 12436426 · doi:10.1002/neu.10151

Nicotine breaks down preformed Alzheimer's beta-amyloid fibrils in vitro

Chemistry / laboratory method, 2002. In test-tube experiments, with no cells, animals or people, researchers tested nicotine and two related chemicals, pyridine and N-methylpyrrolidine, on beta-amyloid. Beta-amyloid is the protein that forms clumps called fibrils in the brains of people with Alzheimer's disease. The more nicotine they added, the more it held back new fibrils from forming and existing fibrils from growing, and it also broke apart fibrils that had already formed. These effects appeared only at nicotine concentrations above 10 mmol/L and were similar to those of N-methylpyrrolidine, which the authors suggest is the part of the nicotine molecule responsible.

Ono K, Hasegawa K, Yamada M et al. (2002). Nicotine breaks down preformed Alzheimer's beta-amyloid fibrils in vitro. Biol Psychiatry. — PubMed PMID: 12399141 · doi:10.1016/s0006-3223(02)01417-8

Chronic nicotine treatment reduces beta-amyloidosis in the brain of a mouse model of Alzheimer's disease (APPsw)

Animal study, 2002. Researchers gave nicotine in drinking fluid for 5.5 months, from 9 to 14.5 months of age, to mice genetically engineered to develop the amyloid plaques seen in Alzheimer's disease. Compared with mice given sucrose, the nicotine-treated mice had more than 80% fewer amyloid beta 1-42 plaques in the brain, and 48% and 60% lower levels of the insoluble amyloid beta 1-40 and 1-42 forms in the cortex. The soluble forms of amyloid beta and a marker of brain support-cell activation did not change. The authors suggest nicotinic drugs may be a possible protective therapy for Alzheimer's disease, but this result is in mice only.

Nordberg A, Hellström-Lindahl E, Lee M et al. (2002). Chronic nicotine treatment reduces beta-amyloidosis in the brain of a mouse model of Alzheimer's disease (APPsw). J Neurochem. — PubMed PMID: 12065674 · doi:10.1046/j.1471-4159.2002.00874.x

Nicotine and neurodegeneration in ageing

Review, 2002. This review looks at how the brain's nicotinic receptors (the receptors nicotine acts on) relate to ageing and dementia. It reports that people with dementia consistently show a marked loss of nicotine binding sites in parts of the brain, which is thought to contribute to memory and thinking problems. The review describes laboratory and animal work, in living animals and in cultured nerve cells, in which nicotine protected nerve cells from damage caused by overactive excitatory chemicals and by beta-amyloid, the main protein in the plaques found in Alzheimer's disease. It also notes that studies of genetically altered animals lacking certain nicotinic receptor types are helping explain how nicotine can both protect nerve cells and harm them.

Zanardi A, Leo G, Biagini G et al. (2002). Nicotine and neurodegeneration in ageing. Toxicol Lett. — PubMed PMID: 12052660 · doi:10.1016/s0378-4274(01)00502-1

Cognitive effects of nicotine

Review, 2001. This review looks at research on how nicotine and other substances that act on nicotinic receptors affect thinking skills. The authors report that nicotine has been found to improve performance on attention and memory tasks. They also report that clinical studies using nicotine skin patches showed benefits for thinking problems linked to Alzheimer's disease, schizophrenia and attention-deficit/hyperactivity disorder (ADHD). In animal studies, the improvement in working memory lasted with long-term exposure, and two types of nicotinic receptors in the hippocampus, a memory area of the brain, were found to be key to these effects.

Rezvani AH, Levin ED (2001). Cognitive effects of nicotine. Biol Psychiatry. — PubMed PMID: 11230877 · doi:10.1016/s0006-3223(00)01094-5

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

Nicotine, brain nicotinic receptors, and neuropsychiatric disorders

Review, 2000. This review describes the nicotinic receptors in the brain, a large family of channels that nicotine acts on, and notes that their normal roles are still not well understood. It summarizes behavioral studies linking these receptors to attention, memory and thinking, and clinical evidence suggesting they are involved in Alzheimer's disease, Parkinson's disease, Tourette's syndrome, schizophrenia and depression. The authors suggest that drugs that switch on these receptors might help prevent some of these disorders, especially Alzheimer's and Parkinson's, or ease their symptoms. They also discuss how these effects might work and describe newer drugs designed to act on specific receptor types.

Mihailescu S, Drucker-Colín R (2000). Nicotine, brain nicotinic receptors, and neuropsychiatric disorders. Arch Med Res. — PubMed PMID: 10880717 · doi:10.1016/s0188-4409(99)00087-9

Nicotine for Alzheimer's disease

Review, 2000. This systematic review looked for high-quality, placebo-controlled trials testing nicotine, given by skin patch or into a vein for more than a day, in people with Alzheimer's disease. No trials met the standard for inclusion, so no results could be combined, and the trials that were looked at were of poor quality. Their data fit equally well with nicotine causing harm, making no difference, or helping. The authors concluded the review could not give reliable evidence that nicotine is a useful treatment for Alzheimer's disease, and they noted nicotine's serious side effects, especially heart and blood-vessel risks in older people and effects on sleep and behavior.

López-Arrieta JM, Rodríguez JL, Sanz F (2000). Nicotine for Alzheimer's disease. Cochrane Database Syst Rev. — PubMed PMID: 10796667 · doi:10.1002/14651858.CD001749

Nicotinic stimulation produces multiple forms of increased glutamatergic synaptic transmission

Cell study, 1998. This laboratory study looked at nerve cells in the hippocampus, a brain area important for learning and memory that carries many nicotinic receptors. Strong, brief activation of these receptors increased signalling through glutamate, one of the brain's main messenger chemicals. One form of the boost lasted only seconds, and another lasted for minutes after the activating drug had been washed away. The effect needed calcium outside the cells and worked through alpha7-type nicotinic receptors on the nerve endings that release glutamate. The authors suggest this may be one way nicotinic activity affects thinking, and that losing these mechanisms may add to the memory problems of Alzheimer's disease. The work was done on isolated brain tissue, not in living people.

Radcliffe KA, Dani JA (1998). Nicotinic stimulation produces multiple forms of increased glutamatergic synaptic transmission. J Neurosci. — PubMed PMID: 9736631 · doi:10.1523/JNEUROSCI.18-18-07075.1998

Nicotinic system involvement in Alzheimer's and Parkinson's diseases. Implications for therapeutics

Review, 1997. This review article discusses nicotinic acetylcholine receptors in the brain and their possible role in Alzheimer's disease and Parkinson's disease, both of which involve a loss of these receptors. It summarizes existing research on nicotine and nicotine-like drugs as potential treatments for cognitive symptoms, noting that while short-term studies have shown promising effects, few long-term studies have tested nicotine or nicotinic drugs in people with dementia, so it remains uncertain whether long-term treatment would produce lasting cognitive benefits or a meaningful difference for patients and families.

Newhouse PA, Potter A, Levin ED (1997). Nicotinic system involvement in Alzheimer's and Parkinson's diseases. Implications for therapeutics. Drugs Aging. — PubMed PMID: 9303280 · doi:10.2165/00002512-199711030-00005

Nicotinic receptor stimulation protects neurons against beta-amyloid toxicity

Cell study, 1997. Researchers grew rat brain nerve cells in the lab and exposed them to beta-amyloid, a protein fragment that builds up in the brains of people with Alzheimer's disease and damages nerve cells. Adding nicotine at the same time greatly reduced the number of cells that died, and a higher nicotine dose gave more protection. This protection went away when drugs that block nicotinic receptors were added, including a blocker of the alpha7 receptor type, and a drug that switches on only alpha7 receptors also protected the cells. The authors suggest that switching on alpha7 nicotinic receptors may help shield nerve cells from beta-amyloid damage, but these results come from cells in a dish, not from animals or people.

Kihara T, Shimohama S, Sawada H et al. (1997). Nicotinic receptor stimulation protects neurons against beta-amyloid toxicity. Ann Neurol. — PubMed PMID: 9266724 · doi:10.1002/ana.410420205

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

Hippocampal synaptic transmission enhanced by low concentrations of nicotine

Cell study, 1996. This laboratory study looked at whether nicotine acts on nicotinic receptors in the hippocampus, a brain area important for learning and memory. By measuring calcium inside single nerve endings in hippocampal tissue, the researchers found that low concentrations of nicotine, acting on receptors that contain the alpha7 subunit, let in enough calcium to trigger the release of chemical messengers and strengthen signals between nerve cells. The work was done on brain tissue in the lab, not in people. The authors suggest this may be one way nicotine affects thinking and memory, and that losing this signalling could help explain memory problems in Alzheimer's disease.

Gray R, Rajan AS, Radcliffe KA et al. (1996). Hippocampal synaptic transmission enhanced by low concentrations of nicotine. Nature. — PubMed PMID: 8878480 · doi:10.1038/383713a0

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

Nicotine therapy in patients with Alzheimer's disease

Review, 1995. This is a discussion piece, not a new experiment, considering whether nicotine could be used as a therapy for Alzheimer's disease. It argues more research is needed on nicotine's long-term effects in these patients, weighs the risks of using a chemical considered a health hazard, and suggests it would be better to develop a similar but less toxic compound. It concludes that until such an alternative exists, a trial of nicotine given through the skin might offer hope and help researchers understand Alzheimer's disease better.

Baldinger SL, Schroeder DJ (1995). Nicotine therapy in patients with Alzheimer's disease. Ann Pharmacother. — PubMed PMID: 7606080 · doi:10.1177/106002809502900315

Chronic nicotine reverses working memory deficits caused by lesions of the fimbria or medial basalocortical projection

Animal study, 1993. Rats were trained on a working-memory maze task, then given surgical cuts to brain pathways (the fimbria or the medial basalocortical projection) that caused their memory performance to decline. Rats given long-term nicotine treatment (via implanted pellets) showed restored choice accuracy, back to the level of unlesioned rats, and nicotine also improved performance in rats without lesions. The paper notes nicotine may be useful for memory problems in diseases like Alzheimer's disease, but this specific finding is from rats, not humans.

Levin ED, Christopher NC, Briggs SJ et al. (1993). Chronic nicotine reverses working memory deficits caused by lesions of the fimbria or medial basalocortical projection. Brain Res Cogn Brain Res. — PubMed PMID: 8257869 · doi:10.1016/0926-6410(93)90021-v

Nicotinic and muscarinic interactions and choice accuracy in the radial-arm maze

Animal study, 1991. Researchers trained 11 adult female rats on a memory task in an eight-arm maze. They then gave the rats nicotine or pilocarpine, a drug that acts on a different type of acetylcholine receptor called muscarinic receptors. Some doses were given alone and some with drugs that block each receptor type. Nicotine significantly improved the rats' choice accuracy, while pilocarpine gave only a marginal improvement; giving both together did not add up to a bigger effect. Blockers of either receptor type reversed the improvement from either drug, more completely for nicotine. These results are only in rats, and the authors suggest the two receptor systems interact in ways that matter for memory and for treating memory problems such as those in Alzheimer's disease.

Levin ED, Rose JE (1991). Nicotinic and muscarinic interactions and choice accuracy in the radial-arm maze. Brain Res Bull. — PubMed PMID: 1933424 · doi:10.1016/0361-9230(91)90293-s

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: Alzheimer's Disease and nicotine (the search this page is built from)

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Connections

• How Memories Form: Synaptic Plasticity (LTP) — 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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