The DOI matches its Crossref record; 212 of the 212 references it cites were found in a registry or an index.
Speed kills: cellular and molecular bases of methamphetamine‐induced nerve terminal degeneration and neuronal apoptosis
Abstract
Methamphetamine (METH) is a drug of abuse that has long been known to damage monoaminergic systems in the mammalian brain. Recent reports have provided conclusive evidence that METH can cause neuropathological changes in the rodent brain via apoptotic mechanisms akin to those reported in various models of neuronal death. The purpose of this review is to provide an interim account for a role of oxygen‐based radicals and the participation of transcription factors and the involvement of cell death genes in METH‐induced neurodegeneration. We discuss data suggesting the participation of endoplasmic reticulum and mitochondria‐mediated activation of caspase‐dependent and ‐independent cascades in the manifestation of METH‐induced apoptosis. Studies that use more comprehensive approaches to gene expression profiling should allow us to draw more instructive molecular portraits of the complex plastic and degenerative effects of this drug.—Cadet, J. L., Jayanthi, S., Deng, X. Speed kills: cellular and molecular bases of methamphetamine‐induced nerve terminal degeneration and neuronal apoptosis. FASEB J. 17, 1775–1788 (2003)
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“Methamphetamine (MA) is a psychostimulant that when used regularly is associated with harms such as injecting and sexual risk-taking behaviour, symptoms of mental ill health (eg, psychosis, aggression, depression and/or anxiety), psychomotor, social and cognitive impairment, criminal activity and sometimes death caused by overdose.1–7”
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Research works printed but not linked: 1
- Cadet J. L., 2003, Gluamate and Addiction, 201
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Clinical trials of N-acetylcysteine in psychiatry and neurology: A systematic review
Deepmala, Slattery, J., Kumar, N., Delhey, L., Berk, M., Dean, O., Spielholz, C., & Frye, R. (2015) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2015.04.015 · Cited by 463
Methamphetamine causes microglial activation in the brains of human abusers
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Self-citationPaulus, M. P., Tapert, S. F., & Schuckit, M. A. (2005) · Archives of General Psychiatry · doi:10.1001/archpsyc.62.7.761 · Cited by 369
Thomas, D. M., Walker, P. D., Benjamins, J. A., Geddes, T. J., & Kuhn, D. M. (2004) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.104.070961 · Cited by 319
Metadata
- Authors
- Cadet, J. L., Jayanthi, S., & Deng, X.
- Affiliations
- National Institutes of Health (US)
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2003-10
- Volume
- 17
- Issue
- 13
- Pages
- 1775-1788
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2083351059
- Cited by
- 286
- References
- 212
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 2 · 2023: 4 · 2022: 6 · 2021: 13 · 2020: 10 · 2019: 10 · 2018: 8 · 2017: 10 · 2016: 8 · 2015: 10 · 2014: 12 · 2013: 10 · 2012: 14
- FWCI
- 1.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The FASEB Journal (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Health and Human Services
- National Institutes of Health
- National Institute on Drug Abuse
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- methamphetamine, neurotoxicity, neuronal apoptosis, nerve terminal degeneration, monoaminergic systems, reactive oxygen species, transcription factors, cell death genes, endoplasmic reticulum stress, mitochondrial dysfunction, caspase activation
- MeSH terms
- Animals, Humans, Methamphetamine, Models, Biological, Nerve Degeneration, Neurons, Signal Transduction, Apoptosis, Presynaptic Terminals, Cytoprotection, Neurotoxicity Syndromes, Mice, Rats
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