Addiction, Adolescence, and Innate Immune Gene Induction
Open accessAbstract
Repeated drug use/abuse amplifies psychopathology, progressively reducing frontal lobe behavioral control, and cognitive flexibility while simultaneously increasing limbic temporal lobe negative emotionality. The period of adolescence is a neurodevelopmental stage characterized by poor behavioral control as well as strong limbic reward and thrill seeking. Repeated drug abuse and/or stress during this stage increase the risk of addiction and elevate activator innate immune signaling in the brain. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a key glial transcription factor that regulates proinflammatory chemokines, cytokines, oxidases, proteases, and other innate immune genes. Induction of innate brain immune gene expression (e.g., NF-κB) facilitates negative affect, depression-like behaviors, and inhibits hippocampal neurogenesis. In addition, innate immune gene induction alters cortical neurotransmission consistent with loss of behavioral control. Studies with anti-oxidant, anti-inflammatory, and anti-depressant drugs as well as opiate antagonists link persistent innate immune gene expression to key behavioral components of addiction, e.g., negative affect-anxiety and loss of frontal-cortical behavioral control. This review suggests that persistent and progressive changes in innate immune gene expression contribute to the development of addiction. Innate immune genes may represent a novel new target for addiction therapy.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Repeated adolescent alcohol exposure can cause neuroinflammation via the release of pro-inflammatory cytokines, which can disrupt synaptic plasticity and lead to neuropathology and cell death.
“Of equal importance is that repeated AAE can cause neuroinflammation via the release of pro-inflammatory cytokines, which can disrupt synaptic plasticity and lead to neuropathology and cell death [37–39].”
From Consequences of adolescent drug use (2023) · cites this paper as [38]
The section “Innate Immune Activation is Involved in Ethanol Drinking, Depression-Like Behavior, and Addiction” reports that chronic intermittent ethanol exposure during adolescence increases inflammatory markers and apoptotic cell death in the neocortex and hippocampus (page unavailable). “Drugs and Stress Induce Innate Immune Genes through Activation of NF-κB Transcription” says ethanol increases pro-inflammatory cytokine expression, but the copy does not establish that cytokine release from repeated adolescent exposure disrupts synaptic plasticity or mediates that cell death. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 126 · Cited by 52
Research works printed but not linked: 1
- Galef B. G. Jr. (1977). “Mechanisms for the social transmission of food preferences from adult to weanling rats,” in Learning Mechanisms in Food Selection, eds. Barker L. M. Best M. Domjan M. (Waco, TX: Baylor University Press), 123– 148
- Authors
- Crews, F. T., & Vetreno, R. P.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Crews, Fulton T.
- Venue
- Frontiers in Psychiatry
- Publisher
- Frontiers Media SA
- Published
- 2011
- Volume
- 2
- Pages
- 19-19
- ISSN
- 1664-0640 (ISSN-L)
- PMC
- PMC3098669
- OpenAlex
- W2056709697
- Cited by
- 52
- References
- 126
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 4 · 2020: 4 · 2019: 5 · 2018: 4 · 2017: 3 · 2016: 5 · 2015: 5 · 2014: 5 · 2013: 4 · 2012: 2
- FWCI
- 1.21
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Psychiatry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Center for Alcohol Studies
- National Institutes of Health (AA-11605, AA007573, AA019767)
- National Institute on Alcohol Abuse and Alcoholism (P50AA011605, U24AA020022, U01AA020023, L40 AA021590, F32AA021040, U24AA020024, U54AA019767, P60AA011605, R28AA012725, T32AA007573)
- Bowles Center for Alcohol Studies, University of North Carolina at Chapel Hill
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- addiction, adolescence, innate immunity, NF-κB, neuroinflammation, drug abuse, stress, behavioral control, negative affect, depression-like behavior, hippocampal neurogenesis, frontal lobe, limbic system, anti-inflammatory agents, opioid antagonists, addiction treatment
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
