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10.1161/STROKEAHA.113.004476 http://scihub22266oqcxt.onion/10.1161/STROKEAHA.113.004476 C4142682!4142682!24938836     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24938836&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Stroke 2014 ; 45 (7): 2093-100 Nephropedia Template TP {{tp|p=24938836|t=2014. Memantine enhances recovery from stroke |pdf=|usr=}}{{24938836}} gab.com Text Memantine enhances recovery from stroke JO: Stroke http://www.kidney.de/pget.php?&tw=1&pmid=24938836 #FOAvip Background and Purpose: Stroke treatment is constrained by limited treatment windows, and the clinical inefficacy of agents that showed preclinical promise. Yet animal and clinical data suggest considerable post-stroke plasticity, which could allow for treatment with recovery-modulating agents. Memantine (MEM) is a well-tolerated N-methyl-D-aspartate (NMDA) glutamate receptor antagonist in common use for Alzheimer's disease. Methods: MEM, 30mg/kg/day, or vehicle, was delivered chronically in drinking water beginning >2 hours after photothrombotic stroke. Results: Though there was no difference in infarct size, behavior, or optical intrinsic signal (OIS) maps in the first seven days after stroke, mice treated chronically with MEM showed significant improvements in motor control, measured by cylinder test and grid walking performance, compared to vehicle treated animals. OIS revealed an increased area of forepaw sensory maps at 28 days after stroke. There was decreased reactive astrogliosis and increased vascular density around the infarcted cortex. Peri-infarct Western blots revealed increased brain-derived neurotrophic factor (BDNF) and phosphorylated-Tropomyosin-related-kinase-B receptor (p-TrkB) expression. Conclusions: Our results suggest that MEM improves stroke outcome in an apparently non-neuroprotective manner involving increased BDNF signaling, reduced reactive astrogliosis and improved vascularization, associated with improved recovery of sensory and motor cortical function. The clinical availability and tolerability of MEM make it an attractive candidate for clinical translation. Twit Text FOAVip Memantine enhances recovery from stroke ????Stroke http://www.kidney.de/pget.php?&tw=1&pmid=24938836 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24938836 #FOAvip English Wikipedia <ref>{{Cite pmid|24938836}}</ref> Memantine enhances recovery from stroke #MMPMID24938836 López-Valdés HE; Clarkson AN; Ao Y; Charles AC; Carmichael ST; Sofroniew MV; Brennan K Stroke 2014[Jul]; 45 (7): 2093-100 PMID24938836show ga Background and Purpose: Stroke treatment is constrained by limited treatment windows, and the clinical inefficacy of agents that showed preclinical promise. Yet animal and clinical data suggest considerable post-stroke plasticity, which could allow for treatment with recovery-modulating agents. Memantine (MEM) is a well-tolerated N-methyl-D-aspartate (NMDA) glutamate receptor antagonist in common use for Alzheimer's disease. Methods: MEM, 30mg/kg/day, or vehicle, was delivered chronically in drinking water beginning >2 hours after photothrombotic stroke. Results: Though there was no difference in infarct size, behavior, or optical intrinsic signal (OIS) maps in the first seven days after stroke, mice treated chronically with MEM showed significant improvements in motor control, measured by cylinder test and grid walking performance, compared to vehicle treated animals. OIS revealed an increased area of forepaw sensory maps at 28 days after stroke. There was decreased reactive astrogliosis and increased vascular density around the infarcted cortex. Peri-infarct Western blots revealed increased brain-derived neurotrophic factor (BDNF) and phosphorylated-Tropomyosin-related-kinase-B receptor (p-TrkB) expression. Conclusions: Our results suggest that MEM improves stroke outcome in an apparently non-neuroprotective manner involving increased BDNF signaling, reduced reactive astrogliosis and improved vascularization, associated with improved recovery of sensory and motor cortical function. The clinical availability and tolerability of MEM make it an attractive candidate for clinical translation. äMemantine enhances recovery from stroke (epmc).pdf DeepDyve Pubget Overpricing