Neurogenetics and Epigenetics in Impulsive Behaviour: Impact on Reward Circuitry

Archer, Trevor; Blum, Kenneth

doi:10.4172/2157-7412.1000115

Cited by 54Neurotransmitter Receptor Influence on BehaviorAttention Deficit Hyperactivity DisorderNeural and Behavioral Psychology Studies

Neurogenetics and Epigenetics in Impulsive Behaviour: Impact on Reward Circuitry

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Archer, Trevor, Blum, Kenneth·2012·Journal of Genetic Syndromes & Gene Therapy

DOI 10.4172/2157-7412.1000115PMC PMC3526005

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Abstract

Adverse, unfavourable life conditions, particularly during early life stages and infancy, can lead to epigenetic regulation of genes involved in stress-response, behavioral disinhibition, and cognitive-emotional systems. Over time, the ultimate final outcome can be expressed through behaviors bedeviled by problems with impulse control, such as eating disorders, alcoholism, and indiscriminate social behavior. While many reward gene polymorphisms are involved in impulsive behaviors, a polymorphism by itself may not translate to the development of a particular behavioral disorder unless it is impacted by epigenetic effects. Brain-derived neurotrophic factor (BDNF) affects the development and integrity of the noradrenergic, dopaminergic, serotonergic, glutamatergic, and cholinergic neurotransmitter systems, and plasma levels of the neurotrophin are associated with both cognitive and aggressive impulsiveness. Epigenetic mechanisms associated with a multitude of environmental factors, including premature birth, low birth weight, prenatal tobacco exposure, non-intact family, young maternal age at birth of the target child, paternal history of antisocial behavior, and maternal depression, alter the developmental trajectories for several neuropsychiatric disorders. These mechanisms affect brain development and integrity at several levels that determine structure and function in resolving the final behavioral expressions.

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Adolescence is a key period of vulnerability for addiction, during which environmental exposures can epigenetically activate or suppress inherited risk factors.
“Adolescence is a key period of vulnerability for addiction, during which environmental exposures can epigenetically activate or suppress inherited risk factors.”
From Beyond Stigma–Integrating Neurobiology, Genetics, and Awareness Integration Theory in Addiction Recovery (2026) · cites this paper as [73]
The Introduction (page unavailable) describes environmental influences on epigenetic gene expression, and its discussion of alcohol abuse links epigenetic changes to addiction vulnerability. But the paper emphasizes prenatal and early-life exposures; it does not identify adolescence as the key period when exposures activate or suppress inherited addiction risk. Its mention of adolescent behavior concerns effects of earlier adversity, not exposures during adolescence. (LLM, conf=0.86)
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Early-life adversity can epigenetically regulate genes involved in behavioral inhibition, stress response, and cognitive control, contributing to the emergence of reward deficiency syndromes.
“Early-life adversity, such as low birth weight, maternal depression, or family instability, can epigenetically regulate genes involved in behavioral inhibition, stress response, and cognitive control, contributing to the emergence of reward deficiency syndromes (RDS).”
From Beyond Stigma–Integrating Neurobiology, Genetics, and Awareness Integration Theory in Addiction Recovery (2026) · cites this paper as [73]
The Conclusions state that early-life adversity may epigenetically regulate genes involved in stress response, behavioral disinhibition, and cognitive-emotional systems. The Introduction says disorders involving impaired inhibition and impulsiveness fit the concept of reward deficiency syndrome, but does not establish that the described epigenetic changes contribute to the emergence of RDS specifically. The Abstract lists low birth weight, maternal depression, and non-intact families among relevant environmental factors; page numbers are unavailable in our copy. (LLM, conf=0.82)
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[6]Archer T Blum K 2011 Epigenetics in neuropsychiatry 1 CRC Press

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Authors: Archer, T., & Blum, K.
Affiliations: University of Gothenburg (SE)
University of Florida (US)
ORCID: Blum, Kenneth
Venue: Journal of Genetic Syndromes & Gene Therapy
Publisher: OMICS Publishing Group
Published: 2012
Volume: 03
Issue: 04
Pages: 1000115-1000115
ISSN: 2157-7412 (ISSN-L)
DOI: 10.4172/2157-7412.1000115
PMC: PMC3526005
OpenAlex: W2168197239
Cited by: 54
References: 242
Citations by year: 2026: 3 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 7 · 2014: 6 · 2013: 7 · 2012: 2
FWCI: 2.90
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Journal of Genetic Syndromes & Gene Therapy (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Alcohol Abuse and Alcoholism (R01AA007112, K05AA000219)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
Keywords: impulsivity, epigenetics, neurogenetics, reward systems, brain-derived neurotrophic factor, genetic polymorphism, childhood adversity, stress response, aggression, eating disorders, alcoholism, social behavior, brain development, neurotransmitter systems, maternal depression, prenatal tobacco exposure, low birth weight, preterm birth

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Neurogenetics and Epigenetics in Impulsive Behaviour: Impact on Reward Circuitry

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