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      Impact of methamphetamine on infection and immunity

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          Abstract

          The prevalence of methamphetamine (METH) use is estimated at ~35 million people worldwide, with over 10 million users in the United States. METH use elicits a myriad of social consequences and the behavioral impact of the drug is well understood. However, new information has recently emerged detailing the devastating effects of METH on host immunity, increasing the acquisition of diverse pathogens and exacerbating the severity of disease. These outcomes manifest as modifications in protective physical and chemical defenses, pro-inflammatory responses, and the induction of oxidative stress pathways. Through these processes, significant neurotoxicities arise, and, as such, chronic abusers with these conditions are at a higher risk for heightened consequences. METH use also influences the adaptive immune response, permitting the unrestrained development of opportunistic diseases. In this review, we discuss recent literature addressing the impact of METH on infection and immunity, and identify areas ripe for future investigation.

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          A review of the clinical pharmacology of methamphetamine.

          To examine the literature regarding clinical pharmacokinetics, direct effects and adverse clinical outcomes associated with methamphetamine use. Relevant literature was identified through a PubMed search. Additional literature was obtained from relevant books and monographs. The mean elimination half-life for methamphetamine is approximately 10 hours, with considerable inter-individual variability in pharmacokinetics. Direct effects at low-to-moderate methamphetamine doses (5-30 mg) include arousal, positive mood, cardiac stimulation and acute improvement in cognitive domains such as attention and psychomotor coordination. At higher doses used typically by illicit users (> or =50 mg), methamphetamine can produce psychosis. Its hypertensive effect can produce a number of acute and chronic cardiovascular complications. Repeated use may induce neurotoxicity, associated with prolonged psychiatric symptoms, cognitive impairment and an increased risk of developing Parkinson's disease. Abrupt cessation of repeated methamphetamine use leads to a withdrawal syndrome consisting of depressed mood, anxiety and sleep disturbance. Acute withdrawal lasts typically for 7-10 days, and residual symptoms associated with neurotoxicity may persist for several months.
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            Methamphetamine use: a comprehensive review of molecular, preclinical and clinical findings.

            Methamphetamine (MA) is a highly addictive psychostimulant drug that principally affects the monoamine neurotransmitter systems of the brain and results in feelings of alertness, increased energy and euphoria. The drug is particularly popular with young adults, due to its wide availability, relatively low cost, and long duration of psychoactive effects. Extended use of MA is associated with many health problems that are not limited to the central nervous system, and contribute to increased morbidity and mortality in drug users. Numerous studies, using complementary techniques, have provided evidence that chronic MA use is associated with substantial neurotoxicity and cognitive impairment. These pathological effects of the drug, combined with the addictive properties of MA, contribute to a spectrum of psychosocial issues that include medical and legal problems, at-risk behaviors and high societal costs, such as public health consequences, loss of family support and housing instability. Treatment options include pharmacological, psychological or combination therapies. The present review summarizes the key findings in the literature spanning from molecular through to clinical effects. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
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              TNF alpha potentiates glutamate neurotoxicity by inhibiting glutamate uptake in organotypic brain slice cultures: neuroprotection by NF kappa B inhibition.

              Glutamate and the proinflammatory cytokine, tumor necrosis factor alpha (TNF alpha), have been suggested to contribute to neurodegenerative diseases. We investigated the interaction of TNF alpha and glutamate on neuronal cell death using fluorescence propidium iodide uptake in rat organotypic hippocampal-entorhinal cortex (HEC) brain slice culture that maintains the cytoarchitecture of the intact brain. Time course and concentration studies indicate that glutamate produced significant neuronal cell death in all four brain areas examined, for example, entorhinal cortex, hippocampal CA1 and CA3 fields, and dentate gyrus. TNF alpha alone at concentration of 20 ng/ml caused little or no detectable neuronal cell death, however, when combined with submaximal glutamate (3.3 mM), TNF alpha significantly increased and accelerated glutamate neurotoxicity. TNF alpha potentiation of glutamate neurotoxicity is blocked by NMDA receptor antagonists but not by AMPA antagonists CNQX and NBQX. Studies directly measuring [14C]-glutamate uptake in HEC slices indicate that TNF alpha dose-dependently inhibited glutamate uptake. Further, inhibitors of glial glutamate transporters potentiated glutamate neurotoxicity similar to TNF alpha. The antioxidant butylated hydroxytoluene (BHT) and the NF kappa B inhibitor PTD-p65 peptide inhibit NF kappa B activation and TNF alpha potentiation of glutamate neurotoxicity. BHT prevented the inhibition of TNFalpha on glutamate transport in HEC slices and also blocked nuclear translocation of NF kappa B subunit p65. These data indicate that TNF alpha and glutamate can act synergistically to induce neuronal cell death. TNF alpha potentiation of glutamate neurotoxicity through the blockade of glutamate transporter activity may represent an important mechanism of neurodegeneration associated with neuroinflammation.
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                Author and article information

                Contributors
                Journal
                Front Neurosci
                Front Neurosci
                Front. Neurosci.
                Frontiers in Neuroscience
                Frontiers Media S.A.
                1662-4548
                1662-453X
                12 January 2015
                2014
                : 8
                : 445
                Affiliations
                [1] 1Department of Biomedical Sciences, Long Island University-Post Brookville, NY, USA
                [2] 2Microbiology and Immunology, Albert Einstein College of Medicine Bronx, NY, USA
                [3] 3Medicine (Division of Infectious Diseases), Albert Einstein College of Medicine Bronx, NY, USA
                [4] 4Department of Biomedical Sciences, NYIT College of Osteopathic Medicine, New York Institute of Technology Old Westbury, NY, USA
                Author notes

                Edited by: Jacob Raber, Oregon Health and Science University, USA

                Reviewed by: Eugene A. Kiyatkin, National Institute on Drug Abuse, USA; Gillian Grafton, University of Birmingham, UK

                *Correspondence: Luis R. Martinez, New York Institute of Technology, College of Osteopathic Medicine, Northern Boulevard, PO Box 8000 Riland Building, Room 28 Old Westbury, NY 11568-8000, USA e-mail: lmarti13@ 123456nyit.edu

                This article was submitted to Neuropharmacology, a section of the journal Frontiers in Neuroscience.

                Article
                10.3389/fnins.2014.00445
                4290678
                25628526
                c75c17a4-4552-4a4e-989e-8b98e920b7dc
                Copyright © 2015 Salamanca, Sorrentino, Nosanchuk and Martinez.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 29 October 2014
                : 17 December 2014
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 162, Pages: 12, Words: 12078
                Categories
                Pharmacology
                Review Article

                Neurosciences
                methamphetamine,infectious diseases,immunity,drug abuse,hiv,neurotoxicity
                Neurosciences
                methamphetamine, infectious diseases, immunity, drug abuse, hiv, neurotoxicity

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