Methamphetamine use: a comprehensive review of molecular, preclinical and clinical findings.
TL;DR: A review of the evidence that chronic MA use is associated with substantial neurotoxicity and cognitive impairment and key findings in the literature spanning from molecular through to clinical effects are summarized.
About: This article is published in Drug and Alcohol Dependence.The article was published on 2013-05-01. It has received 352 citations till now. The article focuses on the topics: Euphoriant & Poison control.
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TL;DR: This review provides a broad-based update of the available literature covering methamphetamine research over the past two decades and concludes with recommendations for future research.
306 citations
Cites background from "Methamphetamine use: a comprehensiv..."
...Furtherore, the present review differs from other methamphetamine eviews (e.g., Panenka et al., 2013) by incorporating this wide ange of domains of interest and by highlighting the increasingly ecognized role for the opioidergic system in the development i.e., reinforcement), maintenance (i.e.,…...
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TL;DR: Results show that MUD is associated with broad cognitive deficits that are in the same range as those associated with alcohol and cocaine use disorder, as recently shown by way of meta-analysis.
195 citations
TL;DR: A systematic overview of drugs that may induce distinct cardiovascular toxicity of illicit sympathomimetic drugs, drugs that prolong the QT interval, antidysrhythmic drugs, digoxin and other cardioactive steroids, beta‐blockers, calcium channel blockers, female hormones, nonsteroidal anti‐inflammatory, and anticancer compounds are discussed.
Abstract: Cardiovascular diseases are a leading cause of morbidity and mortality in most developed countries of the world. Pharmaceuticals, illicit drugs, and toxins can significantly contribute to the overall cardiovascular burden and thus deserve attention. The present article is a systematic overview of drugs that may induce distinct cardiovascular toxicity. The compounds are classified into agents that have significant effects on the heart, blood vessels, or both. The mechanism(s) of toxic action are discussed and treatment modalities are briefly mentioned in relevant cases. Due to the large number of clinically relevant compounds discussed, this article could be of interest to a broad audience including pharmacologists and toxicologists, pharmacists, physicians, and medicinal chemists. Particular emphasis is given to clinically relevant topics including the cardiovascular toxicity of illicit sympathomimetic drugs (e.g., cocaine, amphetamines, cathinones), drugs that prolong the QT interval, antidysrhythmic drugs, digoxin and other cardioactive steroids, beta-blockers, calcium channel blockers, female hormones, nonsteroidal anti-inflammatory, and anticancer compounds encompassing anthracyclines and novel targeted therapy interfering with the HER2 or the vascular endothelial growth factor pathway.
154 citations
TL;DR: 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.
Abstract: 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.
147 citations
Cites background from "Methamphetamine use: a comprehensiv..."
...Methamphetamine (METH) is a kind of highly addictive psychostimulant drug that principally affects themonoamine neurotransmitter systems of the brain and results in feelings of alertness, increasing energy, and euphoria [1]....
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TL;DR: These studies indicate that individuals with a history of chronic methamphetamine abuse often display several signs of corticostriatal dysfunction, including abnormal gray- and white-matter integrity, monoamine neurotransmitter system deficiencies, neuroinflammation, poor neuronal integrity, and aberrant patterns of brain connectivity and function, both when engaged in cognitive tasks and at rest.
139 citations
References
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01 Apr 2003
6,571 citations
TL;DR: The delineation of the neurocircuitry of the evolving stages of the addiction syndrome forms a heuristic basis for the search for the molecular, genetic, and neuropharmacological neuroadaptations that are key to vulnerability for developing and maintaining addiction.
4,160 citations
TL;DR: This review focuses specifically on the links between stress‐related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load.
Abstract: The brain is the key organ of stress reactivity, coping, and recovery processes. Within the brain, a distributed neural circuitry determines what is threatening and thus stressful to the individual. Instrumental brain systems of this circuitry include the hippocampus, amygdala, and areas of the prefrontal cortex. Together, these systems regulate physiological and behavioral stress processes, which can be adaptive in the short-term and maladaptive in the long-term. Importantly, such stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior. In one respect, these bidirectional stress mechanisms are protective in that they promote short-term adaptation (allostasis). In another respect, however, these stress mechanisms can lead to a long-term dysregulation of allostasis in that they promote maladaptive wear-and-tear on the body and brain under chronically stressful conditions (allostatic load), compromising stress resiliency and health. This review focuses specifically on the links between stress-related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load.
1,388 citations
TL;DR: Current issues on the two apparent primary mechanisms--the redistribution of catecholamines from synaptic vesicles to the cytosol, and induction of reverse transport of transmitter through plasma membrane uptake carriers are reviewed.
1,110 citations
"Methamphetamine use: a comprehensiv..." refers background in this paper
...With higher concentrations of amphetamines, this process of reverse transport may not even require binding to the extracellular site of the DAT, as these lipophilic drugs diffuse directly across the plasmalemmal membrane (Mack and Bonisch, 1979; Sulzer et al., 2005)....
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...The mechanism of action of MA and other amphetamines has been described in extensive detail in several excellent reviews (WeilandFiedler et al., 2004; Fleckenstein et al., 2007; Sulzer et al., 2005)....
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TL;DR: Evidence is provided that methamphetamine at dose levels taken by human abusers of the drug leads to dopamine transporter reduction that is associated with motor and cognitive impairment and the urgency of alerting clinicians and the public of the long-term changes that methamphetamine can induce in the human brain.
Abstract: OBJECTIVE: Methamphetamine is a popular and highly addictive drug of abuse that has raised concerns because it has been shown in laboratory animals to be neurotoxic to dopamine terminals. The authors evaluated if similar changes occur in humans and assessed if they were functionally significant. METHOD: Positron emission tomography scans following administration of [11C]d-threo-methylphenidate (a dopamine transporter ligand) measured dopamine transporter levels (a marker of dopamine cell terminals) in the brains of 15 detoxified methamphetamine abusers and 18 comparison subjects. Neuropsychological tests were also performed to assess motor and cognitive function. RESULTS: Methamphetamine abusers showed significant dopamine transporter reduction in the striatum (mean differences of 27.8% in the caudate and 21.1% in the putamen) relative to the comparison subjects; this reduction was evident even in abusers who had been detoxified for at least 11 months. Dopamine transporter reduction was associated with mo...
900 citations