Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, December 20, 2016

CB1 and CB2 Cannabinoid Receptor Antagonists Prevent Minocycline-Induced Neuroprotection Following Traumatic Brain Injury in Mice

It should not be called neuroprotection, it is stopping the neuronal cascade of death. Bet this never gets approved for stroke survivors in the USA. It is better to let survivors stay disabled rather than allow 'Reefer Madness' to take place in our elderly population.
http://cercor.oxfordjournals.org/content/early/2013/08/19/cercor.bht202.abstract
  1. Maria-Paz Viveros1
+ Author Affiliations
  1. 1Faculty of Biology, Department of Animal Physiology (Animal Physiology II), Complutense University of Madrid—Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain,
  2. 2Faculté des Sciences Pharmaceutiques et Biologiques, Laboratoire de Pharmacologie de la Circulation Cérébrale (EA4475),
  3. 3CNRS UMR 8194, UFR Biomédicale des Saints-Pères, Université Paris Descartes, Sorbonne Paris Cité, Paris, France,
  4. 4Pharmacology and Therapeutics, School of Medicine, NCBES Neuroscience Cluster and Centre for Pain Research, National University of Ireland Galway, Galway, Ireland
  5. 5Instituto Cajal, Consejo Superior de Investigaciones Cientificas (CSIC), Madrid, Spain
  1. Address correspondence to Maria-Paz Viveros, Department of Animal Physiology (Animal Physiology II), Faculty of Biology, Complutense University of Madrid, Calle Jose Antonio Novais 2, Madrid 28040, Spain. Email: pazviver@bio.ucm.es

Abstract

Traumatic brain injury (TBI) and its consequences represent one of the leading causes of death in young adults. This lesion mediates glial activation and the release of harmful molecules and causes brain edema, axonal injury, and functional impairment. Since glial activation plays a key role in the development of this damage, it seems that controlling it could be beneficial and could lead to neuroprotective effects. Recent studies show that minocycline suppresses microglial activation, reduces the lesion volume, and decreases TBI-induced locomotor hyperactivity up to 3 months. The endocannabinoid system (ECS) plays an important role in reparative mechanisms and inflammation under pathological situations by controlling some mechanisms that are shared with minocycline pathways. We hypothesized that the ECS could be involved in the neuroprotective effects of minocycline. To address this hypothesis, we used a murine TBI model in combination with selective CB1 and CB2 receptor antagonists (AM251 and AM630, respectively). The results provided the first evidence for the involvement of ECS in the neuroprotective action of minocycline on brain edema, neurological impairment, diffuse axonal injury, and microglial activation, since all these effects were prevented by the CB1 and CB2 receptor antagonists.

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