Substance use disorders: Psychoneuroimmunological mechanisms and new targets for therapy
Open accessAbstract
An estimated 76.4 million people worldwide meet criteria for alcohol use disorders, and 15.3 million meet criteria for drug use disorders. Given the high rates of addiction and the associated health, economic, and social costs, it is essential to develop a thorough understanding of the impact of substance abuse on mental and physical health outcomes and to identify new treatment approaches for substance use disorders (SUDs). Psychoneuroimmunology is a rapidly expanding, multidisciplinary area of research that may be of particular importance to addiction medicine, as its focus is on the dynamic and complex interactions among behavioral factors, the central nervous system, and the endocrine and immune systems (Ader, 2001). This review, therefore, focuses on: 1) the psychoneuroimmunologic effects of SUDs by substance type and use pattern, and 2) the current and future treatment strategies, including barriers that can impede successful recovery outcomes. Evidence-based psychosocial and pharmacotherapeutic treatments are reviewed. Psychological factors and central nervous system correlates that impact treatment adherence and response are discussed. Several novel therapeutic approaches that are currently under investigation are introduced; translational data from animal and human studies is presented, highlighting immunotherapy as a promising new direction for addiction medicine.
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During substance abuse, microglia-mediated neuroinflammation can exert direct neural toxicity and potentially exacerbate addiction via modulation of synapse plasticity.
“Particularly, during substance abuse, microglia-mediated neuroinflammation can exert direct neural toxicity and potentially exacerbate addiction via modulation of synapse plasticity.13, 14”
From Tubular human brain organoids to model microglia-mediated neuroinflammation (2021) · cites this paper as [14]
Section 2.2 (Stimulants; page unavailable) links activated microglia during stimulant exposure to neuroinflammation, neurodegeneration and neuronal damage. Section 2.3 (Opiates; page unavailable) links microglial signaling to morphine-induced reward. Neither passage identifies modulation of synaptic plasticity as the mechanism by which inflammation might exacerbate addiction. (LLM, conf=0.86)
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- Authors
- Loftis, J. M., & Huckans, M.
- Affiliations
- Oregon Health & Science University (US)
- Corresponding author
- Loftis, Jennifer M.
- Venue
- Pharmacology & Therapeutics
- Publisher
- Elsevier BV
- Published
- 2013-08
- Volume
- 139
- Issue
- 2
- Pages
- 289-300
- ISSN
- 0163-7258 (ISSN-L)
- PMC
- PMC3725980
- OpenAlex
- W1980954468
- Cited by
- 47
- References
- 164
- Citations by year
- 2026: 3 · 2024: 2 · 2023: 4 · 2022: 5 · 2021: 9 · 2020: 5 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 2 · 2015: 1 · 2014: 6
- FWCI
- 0.36
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pharmacology & Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (DA018165, P50DA018165)
- Topics
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- substance use disorders, psychoneuroimmunology, alcoholism, drug use disorders, addiction treatment, pharmacotherapy, psychosocial interventions, medication adherence, immunotherapy, immune system, central nervous system, endocrine system, novel therapeutic targets
- MeSH terms
- Animals, Humans, Immunotherapy, Substance-Related Disorders
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