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Author Topic: Methamphetamine Neurotoxicity Mechanisms and Its Molecular Pathophysiology  (Read 1247 times)

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Recent Advances in Methamphetamine Neurotoxicity Mechanisms and Its Molecular Pathophysiology

5 March 2015


Methamphetamine (METH) is a sympathomimeticWiki 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, gliosisWiki, and apoptosisWiki.

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.


Methamphetamine (METH) is a kind of highly addictive psychostimulant drug that principally affects the monoamine neurotransmitter systems of the brain and results in feelings of alertness, increasing energy, and euphoria. The compound was first synthesized from ephedrine in 1893 by the Japanese scientist Nagai Nagayoshi. In 1919, Akira Ogata synthesized crystallized METH by reducing ephedrine using red phosphorous and iodine, providing the basis for production of the drug on a larger scale In 1971, METH was restricted by US law, although oral METH (Ovation Pharmaceuticals) continues to be used today in the USA as a second-line treatment for a number of medical conditions, including attention deficit hyperactivity disorder (ADHD) and refractory obesity.

METH belongs to phenethylamine and amphetamine class of psychoactive drugs. It is an additive pharmacological psychostimulant of the central nervous system (CNS) which results in stimulating excessive dopaminergic transmission in the brain. Ten percent of METH becomes biologically available within ten minutes of smoke inhalation, due to its high lipophilic nature.

METH generates an imbalance in the release and reuptake of dopamine, norepinephrine, and epinephrine producing intense euphoria followed by hours of stimulation, excitation, and alertness. High doses of the METH can damage brain dopamine neurones in experimental animal studies . However, it has been speculated that even low doses used clinically in psychiatry might cause brain damage. Further, an epidemiological study revealed increased risk of development of Parkinson’s disease in hospitalized patients with METH use disorders. However, METH has been indiscriminately used given its high potential for abuse and addiction; this has negatively impacted the public health landscape at multiple levels.

The present research focuses on not only understanding the acute effects of euphoria feelings but also the long-term consequences of their abuse which are rapidly emerging and include evidence of brain injury and neurotoxicity. Although numerous studies have illustrated the deleterious effects of METH on various components of the nervous system, precise cellular and biochemical mechanisms remain largely unknown.

This review will highlight the underlying mechanisms associated with the neurotoxicity of METH and discuss the consequences associated with the neuronal damage produced by the METH. The understanding of the mechanisms involved in METH neurotoxicity could lead to the discovery of new strategies to prevent or counter neurotoxic and neurodegenerative processes.

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I do not condone or support any illegal activities. All information is for theoretical discussion and wonder.
All activities discussed are considered fictional and hypothetical. Information of all discussion has been derived from online research and in the spirit of personal Freedom.


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