Monday, June 23, 2014

Memantine Enhances Recovery From Stroke

And why the f*ck won't your doctor try this after your stroke? I bet any patient would agree to signing the release form. If my doctor had any brains at all he could have asked me to allow immediate administration of statins even though testing had only been proven in rats 3 years prior.
If you want something like this you are going to have to scream at your doctors because they will never try something new that might save a whole slew of your neurons. And what the hell are you paying them for? To sit around and watch your neurons die in the neuronal cascade of death?
http://stroke.ahajournals.org/content/45/7/2093.abstract?etoc
  1. Correspondence to Kevin C. Brennan, MD, 383 Colorow Dr, Room 364, Salt Lake City, UT 84103. E-mail k.c.brennan@hsc.utah.edu.
  1. * Drs López-Valdés and Clarkson contributed equally.

Abstract

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 poststroke plasticity, which could allow treatment with recovery-modulating agents. Memantine is a well-tolerated N-methyl-D-aspartate glutamate receptor antagonist in common use for Alzheimer disease.
Methods—Memantine, 30 mg/kg per day, or vehicle, was delivered chronically in drinking water beginning >2 hours after photothrombotic stroke.
Results—Although there was no difference in infarct size, behavior, or optical intrinsic signal maps in the first 7 days after stroke, mice treated chronically with memantine showed significant improvements in motor control, measured by cylinder test and grid-walking performance, compared with vehicle-treated animals. Optical intrinsic signal 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 and phosphorylated-tropomyosin–related kinase-B receptor expression.
Conclusions—Our results suggest that memantine improves stroke outcomes in an apparently non-neuroprotective manner involving increased brain-derived neurotrophic factor signaling, reduced reactive astrogliosis, and improved vascularization, associated with improved recovery of sensory and motor cortical function. The clinical availability and tolerability of memantine make it an attractive candidate for clinical translation.

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