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.

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The Papers (10)

Newest first. Study types on this page — Human trial: 2 · Animal study: 8. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Developmental Nicotine Exposure Induces Intergenerational Transmission of an Ensemble of Neurodevelopmental Disorder-Related Translatomic Perturbations in DRD1-Expressing Striatal Cells of Adolescent Male Mice

Animal study, 2026. Researchers gave female mice nicotine continuously from before pregnancy, through pregnancy, until their pups were weaned. They then looked at gene activity in one type of brain cell, striatal cells that carry the dopamine D1 receptor, in the male offspring and in the male grand-offspring. In both generations, many genes in these cells were switched on or off differently. Many of those genes are linked to neurodevelopmental disorders such as ADHD, autism and schizophrenia, and some match human genes that show altered DNA methylation in newborns of mothers who smoked. These results come only from mice, and the authors suggest that nicotine-driven changes in how genes are regulated may help explain brain-development problems in the children and grandchildren of mothers who smoke.

Buck JM, Melnick M, Stitzel JA (2026). Developmental Nicotine Exposure Induces Intergenerational Transmission of an Ensemble of Neurodevelopmental Disorder-Related Translatomic Perturbations in DRD1-Expressing Striatal Cells of Adolescent Male Mice. Genes (Basel). — PubMed PMID: 41751513 · doi:10.3390/genes17020128

Nicotine Attenuates Molecular Signalings in the BTBR T+ Itpr3tf/J Mouse Model of Autism

Animal study, 2025. This study looked at a mouse strain that is used as a model of autism. The mice got nicotine in their drinking water for fourteen days and were compared with normal control mice. In the autism-model mice, nicotine lowered several inflammation signals in the blood and reduced inflammatory activity in some immune cells. It also increased the amount of three types of nicotinic receptors in the front part of the brain. A drug that blocks nicotinic receptors reversed one of the immune effects. All of these results come from mice only. The authors suggest that nicotinic receptors play a part in autism and could be a target for future treatments.

AlSharari SD, Mahmood HM, Alasmari AF et al. (2025). Nicotine Attenuates Molecular Signalings in the BTBR T+ Itpr3tf/J Mouse Model of Autism. Mol Neurobiol. — PubMed PMID: 40172818 · doi:10.1007/s12035-025-04894-6

Sperm DNA methylation altered by THC and nicotine: Vulnerability of neurodevelopmental genes with bivalent chromatin

Animal study, 2020. This rat study looked at whether exposure to THC (the main active compound in cannabis) or to nicotine changes DNA methylation, a chemical tag that helps switch genes on and off, in sperm at genes involved in brain development. Seven brain-development genes showed significantly changed methylation in sperm from rats given THC by mouth, and most of these changes were also seen in sperm from rats given THC by injection and from rats exposed to nicotine. The researchers also found that genes linked to autism are more likely to have a particular chromatin structure called bivalent chromatin, which they suggest may make these genes more vulnerable to methylation changes in sperm. These results come from rats only.

Schrott R, Rajavel M, Acharya K et al. (2020). Sperm DNA methylation altered by THC and nicotine: Vulnerability of neurodevelopmental genes with bivalent chromatin. Sci Rep. — PubMed PMID: 32994467 · doi:10.1038/s41598-020-72783-0

The Role of Nicotinic Receptors in the Attenuation of Autism-Related Behaviors in a Murine BTBR T + tf/J Autistic Model

Animal study, 2020. This study looked at a strain of mice used as a model of autism (BTBR mice) and compared them with ordinary lab mice. The mice got nicotine in their drinking water at 50, 100 or 400 mcg/mL for 2 weeks and then went through behaviour tests for social interaction, repetitive grooming, marble burying, movement and balance. At certain doses, nicotine improved sociability and reduced repetitive behaviours in the autism-model mice but had no effect in the ordinary mice, and mecamylamine, a drug that blocks nicotinic receptors, reversed these effects. These results come only from mice, and the authors suggest that drugs targeting nicotinic receptors may be worth studying as a possible autism therapy.

Mahmood HM, Aldhalaan HM, Alshammari TK et al. (2020). The Role of Nicotinic Receptors in the Attenuation of Autism-Related Behaviors in a Murine BTBR T + tf/J Autistic Model. Autism Res. — PubMed PMID: 32691528 · doi:10.1002/aur.2342

Developmental nicotine exposure engenders intergenerational downregulation and aberrant posttranslational modification of cardinal epigenetic factors in the frontal cortices, striata, and hippocampi of adolescent mice

Animal study, 2020. This study looked at mice whose mothers were given nicotine during pregnancy, as a model for smoking or vaping while pregnant, and at the next generation of offspring too. In both the first and second generations of adolescent mice, the researchers found lower levels of several proteins that control how genes are switched on and off (DNMT3A, MeCP2 and HDAC2) in brain regions including the frontal cortex and hippocampus, while another such protein (TET2) was unchanged. They also found abnormal chemical tagging of HDAC2 but not of MeCP2. The authors suggest these changes may help explain how nicotine exposure before birth passes ADHD-, autism- and schizophrenia-like traits across generations, but these results come only from mice.

Buck JM, O'Neill HC, Stitzel JA (2020). Developmental nicotine exposure engenders intergenerational downregulation and aberrant posttranslational modification of cardinal epigenetic factors in the frontal cortices, striata, and hippocampi of adolescent mice. Epigenetics Chromatin. — PubMed PMID: 32138755 · doi:10.1186/s13072-020-00332-0

Developmental nicotine exposure elicits multigenerational disequilibria in proBDNF proteolysis and glucocorticoid signaling in the frontal cortices, striata, and hippocampi of adolescent mice

Animal study, 2019. Researchers gave nicotine in drinking water to female mice during pregnancy and nursing. They then studied the brains and blood of the mice's adolescent offspring (first generation) and grand-offspring (second generation). In both generations, they found an imbalance between BDNF, a protein that supports brain development, and its precursor form, along with less of the enzyme that processes that precursor. They also found reduced activity of the receptor for the stress hormone and low baseline levels of that hormone in the blood. The authors say these changes resemble features of ADHD, autism and schizophrenia and of children whose mothers smoked, but these results come from mice only.

Buck JM, O'Neill HC, Stitzel JA (2019). Developmental nicotine exposure elicits multigenerational disequilibria in proBDNF proteolysis and glucocorticoid signaling in the frontal cortices, striata, and hippocampi of adolescent mice. Biochem Pharmacol. — PubMed PMID: 31404529 · doi:10.1016/j.bcp.2019.08.003

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

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

Modulation of social deficits and repetitive behaviors in a mouse model of autism: the role of the nicotinic cholinergic system

Animal study, 2015. Researchers gave nicotine in drinking water for 4 weeks at four doses (50, 100, 200 or 400 μg/ml) to a mouse strain used as a model of autism and to ordinary lab mice, and measured their behavior before and after. At the lower doses (50 and 100 μg/ml), nicotine increased social interaction in both kinds of mice. At the higher doses it reduced repetitive behavior in the autism-model mice, but at 200 and 400 μg/ml it also lowered their overall physical activity, and at the highest dose they lost weight. These results come from mice only; the authors say the nicotinic receptor system may be a treatment target for social and repetitive-behavior problems in autism.

Wang L, Almeida LE, Spornick NA et al. (2015). Modulation of social deficits and repetitive behaviors in a mouse model of autism: the role of the nicotinic cholinergic system. Psychopharmacology (Berl). — PubMed PMID: 26337613 · doi:10.1007/s00213-015-4058-z

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

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