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10.1155/2015/103969 http://scihub22266oqcxt.onion/10.1155/2015/103969 C4377385!4377385!25861156     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Behav+Neurol 2015 ; 2015 (ä): ä Nephropedia Template TP {{tp|p=25861156|t=2015. Recent Advances in Methamphetamine Neurotoxicity Mechanisms and Its Molecular Pathophysiology |pdf=|usr=}}{{25861156}} gab.com Text Recent Advances in Methamphetamine Neurotoxicity Mechanisms and Its Molecular Pathophysiology JO: Behav Neurol http://www.kidney.de/pget.php?&tw=1&pmid=25861156 #FOAvip 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. Twit Text FOAVip Recent Advances in Methamphetamine Neurotoxicity Mechanisms and Its Molecular Pathophysiology ????Behav Neurol http://www.kidney.de/pget.php?&tw=1&pmid=25861156 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25861156 #FOAvip English Wikipedia <ref>{{Cite pmid|25861156}}</ref> Recent Advances in Methamphetamine Neurotoxicity Mechanisms and Its Molecular Pathophysiology #MMPMID25861156 Yu S; Zhu L; Shen Q; Bai X; Di X Behav Neurol 2015[]; 2015 (ä): ä PMID25861156show ga 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. äRecent Advances in Methamphetamine Neurotoxicity Mechanisms and Its Mo(epmc).pdf DeepDyve Pubget Overpricing