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Behavioural Neurology
Volume 2015 (2015), Article ID 103969, 11 pages
Review Article

Recent Advances in Methamphetamine Neurotoxicity Mechanisms and Its Molecular Pathophysiology

1Department of Neurology, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China
2Department of Neurology, Hospitals of The Armed Police Forces in Hebei, Shijiazhuang 050051, China

Received 9 January 2015; Revised 5 March 2015; Accepted 5 March 2015

Academic Editor: Antonio Pisani

Copyright © 2015 Shaobin Yu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Methamphetamine (METH) is a sympathomimetic amine that belongs to phenethylamine and amphetamine class of psychoactive drugs, which are widely abused for their stimulant, euphoric, empathogenic, and hallucinogenic properties. Many of these effects result from acute increases in dopamine and serotonin neurotransmission. Subsequent to these acute effects, METH produces persistent damage to dopamine and serotonin release in nerve terminals, gliosis, and apoptosis. This review summarized the numerous interdependent mechanisms including excessive dopamine, ubiquitin-proteasome system dysfunction, protein nitration, endoplasmic reticulum stress, p53 expression, inflammatory molecular, D3 receptor, microtubule deacetylation, and HIV-1 Tat protein that have been demonstrated to contribute to this damage. In addition, the feasible therapeutic strategies according to recent studies were also summarized ranging from drug and protein to gene level.