The DOI matches its Crossref record; 168 of the 170 references it cites were found in a registry or an index, and 2 are not checked yet.
The Role of Oxidative Stress, Metabolic Compromise, and Inflammation in Neuronal Injury Produced by Amphetamine-Related Drugs of Abuse
Open accessAbstract
Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) are amphetamine derivatives with high abuse liability. These amphetamine-related drugs of abuse mediate their effects through the acute activation of both dopaminergic and serotonergic neurons. Long-term abuse of these amphetamine derivatives, however, results in damage to both dopaminergic and serotonergic terminals throughout the brain. This toxicity is mediated in part by oxidative stress, metabolic compromise, and inflammation. The overall objective of this review is to highlight experimental evidence that METH and MDMA increase oxidative stress, produce mitochondrial dysfunction, and increase inflammation that converge and culminate in the long-term toxicity to dopaminergic and serotonergic neurons.
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“Several studies have exposed that the long-term use of MPH induces the DA neuron loss and microglia activation causing an increase in pro-inflammatory markers TNFα and IL-1β, among others, resulting in the activation of neuroinflammation and triggering a neurodegenerative process [192, 193].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [193]
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Toxicity of amphetamines: an update
Carvalho, M. C., Carmo, H., Costa, V. M., Capela, J. P., Pontes, H., Remião, F., Carvalho, F. D., & Bastos, M. D. L. (2012) · Archives of Toxicology · doi:10.1007/s00204-012-0815-5 · Cited by 449
Cytokines mediated inflammation and decreased neurogenesis in animal models of depression
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Yamamoto, B. K., Moszczyńska, A., & Gudelsky, G. A. (2010) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.05141.x · Cited by 289
Self-citationThe Effects of Psychostimulant Drugs on Blood Brain Barrier Function and Neuroinflammation
Kousik, S. M., Napier, T. C., & Carvey, P. M. (2012) · Frontiers in Pharmacology · doi:10.3389/fphar.2012.00121 · Cited by 180
Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse
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Metadata
- Authors
- Yamamoto, B. K., & Raudensky, J.
- Affiliations
- Boston University (US)
- Corresponding author
- Yamamoto, Bryan K.
- ORCID
- Yamamoto, Bryan K.
- Venue
- Journal of Neuroimmune Pharmacology
- Published
- 2008-08-15
- Volume
- 3
- Issue
- 4
- Pages
- 203-217
- ISSN
- 1557-1890 (ISSN-L)
- 1557-1904
- PMC
- PMC3955110
- OpenAlex
- W2135980918
- Cited by
- 167
- References
- 168
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 6 · 2023: 6 · 2022: 18 · 2021: 10 · 2020: 8 · 2019: 4 · 2018: 7 · 2017: 10 · 2016: 10 · 2015: 8 · 2014: 12 · 2013: 12 · 2012: 16
- FWCI
- 1.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Neuroimmune Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (R01DA007606)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- methamphetamine, MDMA, ecstasy, oxidative stress, mitochondrial dysfunction, neuroinflammation, dopaminergic neurons, serotonergic neurons, neuronal injury, neurotoxicity, drug abuse
- MeSH terms
- Amphetamines, Animals, Brain, Humans, Inflammation, Neurons, Illicit Drugs, Oxidative Stress
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