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Speed kills: cellular and molecular bases of methamphetamine-induced nerve terminal degeneration and neuronal
Jean Lud Cadet1, Subramaniam Jayanthi, Xiaolin Deng
1Molecular Neuropsychiatry Branch, NIH, NIDA, Intramural Research Program, Department of Health and Human Services, 5500 Nathan Shock Dr., Baltimore, Maryland 21224, USA. jcadet@intra.nida.nih.gov
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.
Insights
Methamphetamine (METH) causes brain damage through apoptosis, involving oxygen radicals and cell death genes. This review details METH-induced neurodegeneration mechanisms, including endoplasmic reticulum and mitochondria pathways.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Methamphetamine (METH) is a neurotoxic drug of abuse.
- METH damages monoaminergic systems in the mammalian brain.
- Evidence indicates METH-induced neuropathological changes occur via apoptosis.
Purpose of the Study:
- To review the role of oxygen radicals in METH neurodegeneration.
- To examine the involvement of transcription factors and cell death genes in METH-induced apoptosis.
- To discuss endoplasmic reticulum and mitochondria-mediated cell death pathways.
Main Methods:
- Review of existing scientific literature on METH neurotoxicity.
- Analysis of studies investigating apoptotic mechanisms.
- Discussion of gene expression profiling approaches.
Main Results:
- METH-induced neurodegeneration involves apoptotic mechanisms.
- Oxygen-based radicals likely participate in METH neurotoxicity.
- Caspase-dependent and -independent cascades are activated via ER and mitochondria.
Conclusions:
- METH triggers neuropathological changes through apoptosis.
- Understanding METH's molecular effects requires comprehensive gene expression analysis.
- Further research into METH's complex cellular impacts is warranted.
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