Nicotine and Autism: The Research
Researchers have studied nicotinic receptors in the autistic brain, the effect of nicotine exposure before birth, and, in small trials, whether nicotine changes some autism symptoms. This page collects the published research on nicotine and autism spectrum disorder, each paper summarised in plain language with its PubMed record.
This collection is research only: papers found on PubMed, each described as its own abstract reports it. Cell and animal results are labelled as such, and harms are listed beside benefits. It is not medical advice.
Table of Contents
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.
The Papers (30)
Newest first. Study types on this page — Human trial: 3 · Human observational study: 4 · Meta-analysis: 1 · Review: 9 · Animal study: 7 · Cell study: 2 · Chemistry / laboratory method: 1 · Other: 3. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.
Deep-Learning-Based Analysis Reveals a Social Behavior Deficit in Mice Exposed Prenatally to Nicotine
Animal study, 2024. Mice exposed to nicotine before birth were tested with deep-learning video tracking tools. These prenatally nicotine-exposed mice showed impulsivity, weaker working memory, higher anxiety, and problems with social interaction, along with fewer new neurons in part of the hippocampus. The findings support the idea that prenatal nicotine exposure is a risk factor for ADHD- and autism-like behavior in mice.
Zhou M, Qiu W, Ohashi N et al. (2024). Deep-Learning-Based Analysis Reveals a Social Behavior Deficit in Mice Exposed Prenatally to Nicotine. Cells. — PubMed PMID: 38334667 · doi:10.3390/cells13030275
A biomarker-based study of prenatal smoking exposure and autism in a Finnish national birth cohort
Human observational study, 2021. This case-control study used Finnish national birth and biobank records to see whether cotinine (a biomarker that nicotine produces in the body) measured in mothers' blood during early pregnancy was linked to autism in their children. Comparing 962 autism cases with matched controls, the researchers found no association between maternal cotinine levels and the odds of autism, whether cotinine was looked at as a continuous measure, by deciles, or by smoking-status categories. The adjusted odds ratio for high versus low cotinine was 0.98, meaning essentially no difference in autism risk between the two groups.
Cheslack-Postava K, Sourander A, Hinkka-Yli-Salomäki S et al. (2021). A biomarker-based study of prenatal smoking exposure and autism in a Finnish national birth cohort. Autism Res. — PubMed PMID: 34505741 · doi:10.1002/aur.2608
A Neural Network Reveals Motoric Effects of Maternal Preconception Exposure to Nicotine on Rat Pup Behavior: A New Approach for Movement Disorders Diagnosis
Animal study, 2021. Researchers gave female rats nicotine in their drinking water for seven weeks before mating, then used a computer program (a deep neural network) to analyze the movement of their 10-day-old pups in an open-field test. The computer program was better than standard human-designed measures at telling apart pups born to nicotine-exposed mothers from pups born to unexposed mothers (87% versus 64% accuracy), and it picked up new differences in posture, how pups started moving, and repeated "warm-up" movement patterns. The study concludes that nicotine exposure in mothers before pregnancy delayed and changed how their pups' motor skills developed, and notes these movement patterns resemble ones seen in some neurodevelopmental conditions in children.
Torabi R, Jenkins S, Harker A et al. (2021). A Neural Network Reveals Motoric Effects of Maternal Preconception Exposure to Nicotine on Rat Pup Behavior: A New Approach for Movement Disorders Diagnosis. Front Neurosci. — PubMed PMID: 34354562 · doi:10.3389/fnins.2021.686767
Curcumin Potentiates α7 Nicotinic Acetylcholine Receptors and Alleviates Autistic-Like Social Deficits and Brain Oxidative Stress Status in Mice
Animal study, 2021. Researchers studied curcumin (the active compound in turmeric), which can boost the activity of a brain receptor also activated by nicotine (the alpha-7 nicotinic acetylcholine receptor). In lab-dish nerve cell recordings, curcumin strengthened signals through this receptor. In mice bred to show autism-like traits, curcumin injections reduced social deficits and lowered markers of oxidative stress in the brain, without affecting the mice's general movement or anxiety-like behavior.
Jayaprakash P, Isaev D, Shabbir W et al. (2021). Curcumin Potentiates α7 Nicotinic Acetylcholine Receptors and Alleviates Autistic-Like Social Deficits and Brain Oxidative Stress Status in Mice. Int J Mol Sci. — PubMed PMID: 34298871 · doi:10.3390/ijms22147251
An Evolving Therapeutic Rationale for Targeting the α7 Nicotinic Acetylcholine Receptor in Autism Spectrum Disorder
Review, 2020. This is a review discussing the alpha7 nicotinic acetylcholine receptor, which responds to acetylcholine and nicotine, as a possible target for treating autism spectrum disorder. It summarizes findings that people with autism show abnormalities in brain cholinergic signaling, that a genetic deletion affecting the gene for this receptor is linked to autism-spectrum conditions, and that in mouse models of autism the receptor helps regulate certain brain cells involved in brain-wave synchronization tied to memory and brain connectivity. The paper reviews existing research and argues for future clinical trials of drugs that selectively target this receptor in people with autism, but does not itself report new experimental results.
Deutsch SI, Burket JA (2020). An Evolving Therapeutic Rationale for Targeting the α7 Nicotinic Acetylcholine Receptor in Autism Spectrum Disorder. Curr Top Behav Neurosci. — PubMed PMID: 32468495 · doi:10.1007/7854_2020_136
Genome-Wide Meta-Analyses of FTND and TTFC Phenotypes
Human observational study, 2020. Researchers analyzed genetic data from over 19,000 adult smokers across 14 study groups to look for gene variants linked to two measures of nicotine dependence: a dependence questionnaire score and how soon after waking someone smokes their first cigarette. They found several candidate genes associated with these traits, though attempts to confirm the top new findings in a separate smaller group of smokers did not reach statistical significance. Some of the genes that showed up for both dependence measures, including one for a nicotine receptor subunit, had also previously been linked to other addictions (alcohol, cocaine, heroin) and to autism and schizophrenia.
Chen J, Loukola A, Gillespie NA et al. (2020). Genome-Wide Meta-Analyses of FTND and TTFC Phenotypes. Nicotine Tob Res. — PubMed PMID: 31294817 · doi:10.1093/ntr/ntz099
An Exploratory Trial of Transdermal Nicotine for Aggression and Irritability in Adults with Autism Spectrum Disorder
Human trial, 2018. This small trial tested whether a low-dose nicotine skin patch could reduce aggression and irritability in adults with autism, based on the idea that nicotinic receptors, especially the alpha-7 type, play a role in both autism and aggressive behavior. Eight adults were randomly assigned to wear a 7 mg nicotine patch for one week and a placebo patch for another week, without knowing which was which. All participants tolerated the nicotine patch well, and among the five people whose data could be used for the main measure, irritability scores improved more with nicotine than with placebo. Sleep ratings also improved with nicotine and tracked with the drop in irritability. The authors say these early results justify more research and are not proof that the treatment works.
Lewis AS, van Schalkwyk GI, Lopez MO et al. (2018). An Exploratory Trial of Transdermal Nicotine for Aggression and Irritability in Adults with Autism Spectrum Disorder. J Autism Dev Disord. — PubMed PMID: 29536216 · doi:10.1007/s10803-018-3536-7
Basolateral amygdala and stress-induced hyperexcitability affect motivated behaviors and addiction
Review, 2017. This is a review paper discussing how a brain region called the basolateral amygdala processes stress, fear, and reward, and how disrupted signaling there relates to conditions like PTSD, autism, ADHD, and drug addiction. It focuses heavily on animal studies of nicotine-seeking behavior, describing how chronic stress makes neurons in this brain region overactive and how this circuit is involved in nicotine intake, nicotine-seeking after stress, and relapse to nicotine use, drawing on both animal models and some human brain imaging and behavioral research.
Sharp BM (2017). Basolateral amygdala and stress-induced hyperexcitability affect motivated behaviors and addiction. Transl Psychiatry. — PubMed PMID: 28786979 · doi:10.1038/tp.2017.161
Maternal smoking and autism spectrum disorder: meta-analysis with population smoking metrics as moderators
Meta-analysis, 2017. This meta-analysis pooled 22 observational studies covering about 795,632 cases and 1,829,256 controls to look at whether mothers smoking during pregnancy was linked to autism spectrum disorder in their children. Overall, the pooled result found no significant association (odds ratio 1.16). However, when the researchers also factored in each country's adult male smoking rate as a stand-in for secondhand smoke exposure, a significant relationship emerged, suggesting population-level smoking patterns matter. The authors note they cannot rule out that paternal or secondhand nicotine exposure, rather than maternal exposure during pregnancy, could explain the findings.
Jung Y, Lee AM, McKee SA et al. (2017). Maternal smoking and autism spectrum disorder: meta-analysis with population smoking metrics as moderators. Sci Rep. — PubMed PMID: 28659613 · doi:10.1038/s41598-017-04413-1
Altered nocifensive behavior in animal models of autism spectrum disorder: The role of the nicotinic cholinergic system
Animal study, 2016. Researchers looked at how two mouse strains used as models of autism respond to pain, and how nicotine changes that response. Both autism-model strains reacted less than normal mice to painful heat and to electrical stimulation of one type of pain nerve fiber. They reacted normally to stimulation of other fiber types and more strongly to belly pain caused by an acetic acid injection. In one of the strains, low doses of nicotine increased the time the mice took to react to a hot plate and high doses decreased it, while in normal mice nicotine reduced heat pain only at the high dose. The autism-model mice also had lower levels of several nicotinic receptor subunits in parts of the brain, both before birth and in adulthood. The authors suggest these receptors may be a treatment target for behavior and sensory problems in autism, but all of these results come from mice only.
Wang L, Almeida LE, Nettleton M et al. (2016). Altered nocifensive behavior in animal models of autism spectrum disorder: The role of the nicotinic cholinergic system. Neuropharmacology. — PubMed PMID: 27638450 · doi:10.1016/j.neuropharm.2016.09.013
Brief Report: Initial Trial of Alpha7-Nicotinic Receptor Stimulation in Two Adult Patients with Autism Spectrum Disorder
Human trial, 2016. Two adults with autism spectrum disorder took part in a small double-blind, placebo-controlled crossover trial testing a drug that specifically stimulates the alpha7-nicotinic receptor, a receptor that nicotine also acts on and that has been linked to genetic changes in autism. A brain-wave test and cognitive testing showed the drug produced the intended effect on brain signaling and on a measure of thinking ability, and both patients reported feeling more attentive on their own ratings.
Olincy A, Blakeley-Smith A, Johnson L et al. (2016). Brief Report: Initial Trial of Alpha7-Nicotinic Receptor Stimulation in Two Adult Patients with Autism Spectrum Disorder. J Autism Dev Disord. — PubMed PMID: 27565651 · doi:10.1007/s10803-016-2890-6
Varenicline in Autism: Theory and Case Report of Clinical and Biochemical Changes
Other, 2016. This case report describes a 19-year-old man with severe autism who was given low-dose varenicline, a drug that acts on the same nicotinic receptors that nicotine acts on. With treatment his clinical symptoms improved and several biochemical markers in his saliva and urine (including dopamine and related substances) moved toward normal levels. When the drug was stopped he got worse, and when it was restarted he improved again; he stayed on it for over a year without noticeable side effects.
Mostafavi M, Hardy P, Arnold LE (2016). Varenicline in Autism: Theory and Case Report of Clinical and Biochemical Changes. J Child Adolesc Psychopharmacol. — PubMed PMID: 27123827 · doi:10.1089/cap.2015.0230
The α4β2 nicotinic acetylcholine receptor modulates autism-like behavioral and motor abnormalities in pentylenetetrazol-kindled mice
Animal study, 2016. Mice were given a drug (pentylenetetrazol) to trigger repeated seizures, which caused problems with movement coordination, anxiety-like behavior, and reduced social approach -- behaviors the researchers compare to autism and ADHD. Treating these seizure-prone mice with a nicotinic receptor-activating drug called ABT-418 lessened these movement, anxiety, and social problems. The seizure-prone mice also had less of a nicotinic receptor protein and more of another protein (neuroligin 3) in a brain region called the piriform cortex, and the researchers suggest these changes are linked to the autism-like and ADHD-like behaviors.
Takechi K, Suemaru K, Kiyoi T et al. (2016). The α4β2 nicotinic acetylcholine receptor modulates autism-like behavioral and motor abnormalities in pentylenetetrazol-kindled mice. Eur J Pharmacol. — PubMed PMID: 26868186 · doi:10.1016/j.ejphar.2016.02.021
The 15q13.3 deletion syndrome: Deficient α(7)-containing nicotinic acetylcholine receptor-mediated neurotransmission in the pathogenesis of neurodevelopmental disorders
Review, 2016. This review discusses a genetic condition caused by a small deletion on chromosome 15 that removes a gene called CHRNA7, which codes for a nicotinic receptor subunit (the alpha-7 nicotinic acetylcholine receptor) that nicotine acts on. People with this deletion can develop conditions such as epilepsy, intellectual disability, autism spectrum disorders, and schizophrenia. The paper discusses drugs called positive allosteric modulators that enhance this receptor's activity as a potential treatment approach being studied in clinical trials for autism spectrum disorders and schizophrenia, including in patients without the genetic deletion.
Deutsch SI, Burket JA, Benson AD et al. (2016). The 15q13.3 deletion syndrome: Deficient α(7)-containing nicotinic acetylcholine receptor-mediated neurotransmission in the pathogenesis of neurodevelopmental disorders. Prog Neuropsychopharmacol Biol Psychiatry. — PubMed PMID: 26257138 · doi:10.1016/j.pnpbp.2015.08.001
Desformylflustrabromine Modulates α4β2 Neuronal Nicotinic Acetylcholine Receptor High- and Low-Sensitivity Isoforms at Allosteric Clefts Containing the β2 Subunit
Cell study, 2015. Researchers used frog egg cells (Xenopus oocytes) to study how a compound called dFBr boosts the activity of a nicotinic acetylcholine receptor subtype made of alpha4 and beta2 subunits, which responds to acetylcholine and nicotine and is linked to conditions including autism, nicotine addiction, Alzheimer's disease, and Parkinson's disease. By changing one amino acid at a time on the beta2 subunit, they found that one specific change essentially eliminated dFBr's boosting effect, and several other changes altered how strongly dFBr worked, pointing to a particular region of the receptor involved in this effect.
Weltzin MM, Schulte MK (2015). Desformylflustrabromine Modulates α4β2 Neuronal Nicotinic Acetylcholine Receptor High- and Low-Sensitivity Isoforms at Allosteric Clefts Containing the β2 Subunit. J Pharmacol Exp Ther. — PubMed PMID: 26025967 · doi:10.1124/jpet.115.223933
Reduction of Aggressive Episodes After Repeated Transdermal Nicotine Administration in a Hospitalized Adolescent with Autism Spectrum Disorder
Human trial, 2015. This is a case report about one teenager with autism spectrum disorder who was in the hospital because of aggressive episodes. Doctors added a nicotine skin patch to the teen's other medicines. The patch was well tolerated each time it was used, and the teen needed emergency medication and physical restraint less often. The authors say these findings call for more study of nicotine patches for aggression in autism.
Van Schalkwyk GI, Lewis AS, Qayyum Z et al. (2015). Reduction of Aggressive Episodes After Repeated Transdermal Nicotine Administration in a Hospitalized Adolescent with Autism Spectrum Disorder. J Autism Dev Disord. — PubMed PMID: 25982311 · doi:10.1007/s10803-015-2471-0
Nicotinic ACh receptors as therapeutic targets in CNS disorders
Review, 2015. This review discusses nicotinic acetylcholine receptors, the brain proteins that nicotine acts on, and their role in regulating brain cell activity. It describes how these receptors are involved in processes like anxiety, pain processing, food intake, and thinking skills, and discusses their potential as treatment targets in brain conditions including Alzheimer's disease, autism, schizophrenia, and nerve pain.
Dineley KT, Pandya AA, Yakel JL (2015). Nicotinic ACh receptors as therapeutic targets in CNS disorders. Trends Pharmacol Sci. — PubMed PMID: 25639674 · doi:10.1016/j.tips.2014.12.002
Defining the putative inhibitory site for a selective negative allosteric modulator of human α4β2 neuronal nicotinic receptors
Other, 2012. This study used molecular engineering techniques to map the binding site of a lab compound that selectively blocks human α4β2 nicotinic acetylcholine receptors, the same receptor subtype thought to be involved in nicotine addiction. By altering specific amino acids on the receptor, researchers identified three (Phe118, Glu60, and Thr58) that are important for this blocking compound's action, and used related chemical variants to understand which molecular features affect how strongly a compound binds there.
Henderson BJ, González-Cestari TF, Yi B et al. (2012). Defining the putative inhibitory site for a selective negative allosteric modulator of human α4β2 neuronal nicotinic receptors. ACS Chem Neurosci. — PubMed PMID: 23019495 · doi:10.1021/cn300035f
Genetic architectures of psychiatric disorders: the emerging picture and its implications
Review, 2012. This review discusses genetics research across nine major psychiatric conditions, including nicotine dependence, alongside disorders like schizophrenia, bipolar disorder, and autism spectrum disorder. It summarizes progress made over five years in understanding the genetic architecture of these conditions as a group, rather than focusing in depth on nicotine dependence specifically.
Sullivan PF, Daly MJ, O'Donovan M (2012). Genetic architectures of psychiatric disorders: the emerging picture and its implications. Nat Rev Genet. — PubMed PMID: 22777127 · doi:10.1038/nrg3240
Pharmacotherapeutic implications of the association between genomic instability at chromosome 15q13.3 and autism spectrum disorders
Review, 2011. This review discusses a genetic deletion on chromosome 15 that is linked to autism spectrum disorders and that removes one copy of a gene coding for the alpha7 nicotinic acetylcholine receptor, a receptor that nicotine acts on. The authors argue there is a scientific rationale for testing drugs that activate this receptor in people with autism, including receptor-stimulating compounds related to nicotine, and propose that early-stage clinical trials could explore effects on attention, cognition and memory. No new patient data are presented; this is a reasoning-based proposal for future research.
Deutsch SI, Urbano MR, Burket JA et al. (2011). Pharmacotherapeutic implications of the association between genomic instability at chromosome 15q13.3 and autism spectrum disorders. Clin Neuropharmacol. — PubMed PMID: 22094647 · doi:10.1097/WNF.0b013e31823a1247
Cerebellar nicotinic cholinergic receptors are intrinsic to the cerebellum: implications for diverse functional roles
Animal study, 2011. Researchers studied nicotinic receptors in the cerebellum of lab animals using chemical lesion models and electrophysiology recordings in brain slices. They found that these nicotinic receptors are made by cells within the cerebellum itself, rather than being delivered there from other brain regions, and that one specific receptor subtype (beta4-containing) can regulate inhibitory signaling between two major types of cerebellar neurons.
Turner JR, Ortinski PI, Sherrard RM et al. (2011). Cerebellar nicotinic cholinergic receptors are intrinsic to the cerebellum: implications for diverse functional roles. Cerebellum. — PubMed PMID: 21562921 · doi:10.1007/s12311-011-0285-y
Cholinergic abnormalities in autism: is there a rationale for selective nicotinic agonist interventions?
Review, 2010. This review paper looks at evidence that brain acetylcholine systems, especially nicotinic acetylcholine receptors, are abnormal in people with autism spectrum disorders, based mainly on small postmortem tissue studies. The authors argue that because the alpha7 nicotinic receptor sits on inhibitory brain cells, selectively stimulating it might boost inhibitory signaling and could be worth testing, and they call for clinical trials of drugs that target nicotinic receptors as a possible treatment approach.
Deutsch SI, Urbano MR, Neumann SA et al. (2010). Cholinergic abnormalities in autism: is there a rationale for selective nicotinic agonist interventions?. Clin Neuropharmacol. — PubMed PMID: 20190638 · doi:10.1097/WNF.0b013e3181d6f7ad
Presynaptic targeting of alpha4beta 2 nicotinic acetylcholine receptors is regulated by neurexin-1beta
Cell study, 2009. Researchers studied brain cells (from rats and lab-grown human-derived cells) to learn how a type of nicotine receptor called alpha4beta2 gets positioned at the junctions between neurons. They found a protein called neurexin-1beta binds to this receptor and helps direct it to the correct location on nerve cells, working together with a partner protein called neuroligin-1. The paper notes that problems with the human neurexin-1 gene have been linked to nicotine dependence and to autism spectrum disorders, and suggests this receptor-targeting mechanism could help explain how those gene problems might contribute to both conditions.
Cheng SB, Amici SA, Ren XQ et al. (2009). Presynaptic targeting of alpha4beta 2 nicotinic acetylcholine receptors is regulated by neurexin-1beta. J Biol Chem. — PubMed PMID: 19567877 · doi:10.1074/jbc.M109.017384
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
Nicotinic cholinergic antagonists: a novel approach for the treatment of autism
Review, 2006. This 2006 paper is a hypothesis article proposing that drugs blocking nicotinic acetylcholine receptors (the same receptors nicotine activates) might help treat autism, rather than drugs that mimic nicotine. The author notes that autistic people smoke less than the general population and suggests this is because their brains already have overactive cholinergic signaling, so blocking these receptors rather than stimulating them might ease symptoms. It cites anecdotal reports from one doctor that mecamylamine, a drug that blocks these receptors, helped some autistic symptoms, and calls for controlled clinical trials to test this idea.
Lippiello PM (2006). Nicotinic cholinergic antagonists: a novel approach for the treatment of autism. Med Hypotheses. — PubMed PMID: 16406687 · doi:10.1016/j.mehy.2005.11.015
Executive and social behaviors under nicotinic receptor regulation
Animal study, 2003. This study in mice looked at how nicotinic receptors affect complex behaviors like organizing movement sequences, resolving conflict, and social interaction. Mice lacking the beta2 nicotinic receptor subunit showed deficits in these higher-order behaviors while simpler, automatic motor behaviors stayed normal. The researchers note these deficits resemble the rigid and asocial behavior patterns seen in some psychological disorders, including autism and ADHD.
Granon S, Faure P, Changeux JP (2003). Executive and social behaviors under nicotinic receptor regulation. Proc Natl Acad Sci U S A. — PubMed PMID: 12876201 · doi:10.1073/pnas.1533498100
Low prevalence of smoking in patients with autism spectrum disorders
Human observational study, 2003. Researchers compared smoking rates in 95 people with autism spectrum disorders to the general population and to 161 people with schizophrenia-spectrum disorders. Only 12.6% of the autism group smoked, compared with 19% in the general population and 47% in the schizophrenia group, suggesting smoking is unusually rare among people with autism.
Bejerot S, Nylander L (2003). Low prevalence of smoking in patients with autism spectrum disorders. Psychiatry Res. — PubMed PMID: 12860373 · doi:10.1016/s0165-1781(03)00123-9
Cholinergic activity in autism: abnormalities in the cerebral cortex and basal forebrain
Human observational study, 2001. Researchers examined brain tissue from deceased autistic adults compared with non-autistic adults and nonautistic adults with mental retardation. In the autistic group, nicotinic receptor binding was 65%-73% lower in two areas of the cerebral cortex, with lower levels of two nicotinic receptor subunits also found. A related receptor type was also somewhat lower in one brain region. The autistic group's basal forebrain showed three times higher levels of a nerve growth factor compared to the normal group.
Perry EK, Lee ML, Martin-Ruiz CM et al. (2001). Cholinergic activity in autism: abnormalities in the cerebral cortex and basal forebrain. Am J Psychiatry. — PubMed PMID: 11431227 · doi:10.1176/appi.ajp.158.7.1058
Nicotinic receptors in human brain: topography and pathology
Review, 2000. This is a review of brain nicotinic acetylcholine receptors, the proteins that nicotine acts on. It describes how these receptor subtypes are highly expressed early in human brain development and how specific subunit deficits have been reported in connection with several conditions, including a deficit in the alpha4beta2 subtype linked to autism and in alpha7 (and possibly alpha4beta2) linked to schizophrenia; other subunit changes are described in aging, Alzheimer's disease, and Parkinson's disease. The authors note that nicotinic-based therapies might help some neurological conditions, but say more research is needed to link specific receptor deficits to symptoms before this can guide treatment.
Court JA, Martin-Ruiz C, Graham A et al. (2000). Nicotinic receptors in human brain: topography and pathology. J Chem Neuroanat. — PubMed PMID: 11207426 · doi:10.1016/s0891-0618(00)00110-1
Functional analysis and treatment of cigarette pica
Other, 1996. This case report describes a young man with intellectual disability and autism who repeatedly ate cigarette butts (a behavior called pica). Testing showed he kept eating cigarettes containing nicotine but not herbal cigarettes without nicotine, and he preferred tobacco over the cigarette's other parts like paper and filter. A functional analysis showed this eating behavior happened regardless of any social attention, and a treatment designed to break the connection between the behavior and its reward reduced his cigarette consumption to zero.
Piazza CC, Hanley GP, Fisher WW (1996). Functional analysis and treatment of cigarette pica. J Appl Behav Anal. — PubMed PMID: 8995829 · doi:10.1901/jaba.1996.29-437
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Connections
- 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