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10.1586/14737175.2014.960399 http://scihub22266oqcxt.onion/10.1586/14737175.2014.960399 C4479119!4479119!25220836     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Expert+Rev+Neurother 2014 ; 14 (10): 1115-7 Nephropedia Template TP {{tp|p=25220836|t=2014. VMAT2 and Parkinson?s disease: harnessing the dopamine vesicle |pdf=|usr=}}{{25220836}} gab.com Text VMAT2 and Parkinson s disease: harnessing the dopamine vesicle JO: Expert Rev Neurother http://www.kidney.de/pget.php?&tw=1&pmid=25220836 #FOAvip Despite a movement away from dopamine-focused Parkinson?s disease (PD) research, a recent surge of evidence now suggests that altered vesicular storage of dopamine may contribute to the demise of the nigral neurons in this disease. Human studies demonstrate that the vesicular monoamine transporter 2 (VMAT2; SLC18A2) is dysfunctional in PD brain. Moreover, studies with transgenic mice suggest that there is an untapped reserve capacity of the dopamine vesicle that could be unbridled by increasing VMAT2 function. Therapeutic manipulation of VMAT2 level or function has the potential to improve efficacy of dopamine derived from administered levodopa, increase dopamine neurotransmission from remaining midbrain dopamine neurons and protect against neurotoxic insults. Thus, the development of drugs to enhance the storage of release of dopamine may be a fruitful avenue of research for PD. Twit Text FOAVip VMAT2 and Parkinson s disease: harnessing the dopamine vesicle ????Expert Rev Neurother http://www.kidney.de/pget.php?&tw=1&pmid=25220836 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25220836 #FOAvip English Wikipedia <ref>{{Cite pmid|25220836}}</ref> VMAT2 and Parkinson?s disease: harnessing the dopamine vesicle #MMPMID25220836 Lohr KM; Miller GW Expert Rev Neurother 2014[Oct]; 14 (10): 1115-7 PMID25220836show ga Despite a movement away from dopamine-focused Parkinson?s disease (PD) research, a recent surge of evidence now suggests that altered vesicular storage of dopamine may contribute to the demise of the nigral neurons in this disease. Human studies demonstrate that the vesicular monoamine transporter 2 (VMAT2; SLC18A2) is dysfunctional in PD brain. Moreover, studies with transgenic mice suggest that there is an untapped reserve capacity of the dopamine vesicle that could be unbridled by increasing VMAT2 function. Therapeutic manipulation of VMAT2 level or function has the potential to improve efficacy of dopamine derived from administered levodopa, increase dopamine neurotransmission from remaining midbrain dopamine neurons and protect against neurotoxic insults. Thus, the development of drugs to enhance the storage of release of dopamine may be a fruitful avenue of research for PD. äVMAT2 and Parkinson?s disease: harnessing the dopamine vesicle (epmc).pdf DeepDyve Pubget Overpricing