Cited by 286Cell death mechanisms and regulationNeurotransmitter Receptor Influence on BehaviorParkinson's Disease Mechanisms and Treatments

Speed kills: cellular and molecular bases of methamphetamine‐induced nerve terminal degeneration and neuronal apoptosis

Cadet, Jean Lud, Jayanthi, Subramaniam, Deng, Xiaolin·2003·The FASEB Journal

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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Crossref · 10.1096/fj.03-0073rev

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212 of 212 references verified0 citation errors · 0 not checkable

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  • Methamphetamine use, when regular, is associated with harms including injecting and sexual risk-taking behaviour, symptoms of mental ill health (psychosis, aggression, depression, anxiety), psychomotor, social and cognitive impairment, criminal activity, and sometimes death by overdose.

    “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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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 › 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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