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

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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

DOI 10.1096/fj.03-0073rev

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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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Authors: Cadet, J. L., Jayanthi, S., & Deng, X.
Affiliations: National Institutes of Health (US)
ORCID: Cadet, Jean Lud
Jayanthi, Subramaniam
Deng, Xiaolin
Venue: The FASEB Journal
Publisher: Wiley
Published: 2003-10
Volume: 17
Issue: 13
Pages: 1775-1788
ISSN: 0892-6638 (ISSN-L)
1530-6860
DOI: 10.1096/fj.03-0073rev
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
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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Speed kills: cellular and molecular bases of methamphetamine‐induced nerve terminal degeneration and neuronal apoptosis

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