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.

Wednesday, February 25, 2015

Neurons cool off - Synaptic reestablishment

This seems like a useful occurrence post-stroke. What will it take for your doctor to follow up with a clinical trial to prove it one way or another? Or does your doctor not have any goals around solving problems in stroke because your hospital president has failed at leading?

"You can judge a leader by the size of the problems they tackle."

http://stm.sciencemag.org/content/7/276/276ec33.full? 

  1. Anne Schaefer
+ Author Affiliations
  1. Friedman Brain Institute, Department of Neuroscience and Department of Psychiatry, Mount Sinai School of Medicine, New York, NY 10029, USA. E-mail: anne.schaefer@mssm.edu
It’s common wisdom that a cold shower is good for your health. Now, Peretti et al. show that Rbm3, a protein induced by cold shock, triggers neurons to form new synapses.
Low body temperature in hibernating mammals leads to a reversible loss of synaptic contacts that are efficiently re-established upon rewarming. Using electron microscopy, Peretti et al. report that the induction of a hibernation-like body temperature in mice for as little as 45 minutes caused a similar loss of synaptic connections that were regained upon rewarming the animals. This capacity for synaptic regeneration after cold trauma was lost in mice suffering from two neurodegenerative diseases. The impaired cooling-induced regeneration of synapses in mice suffering from either prion-like disease or Alzheimer’s disease was associated with a decrease in one of the known cold-shock proteins, the RNA-binding motif protein RBM3. The authors show that RNAi-based knockdown of RBM3 exacerbated the loss of synapses in both disease models and accelerated disease progression. Conversely, the enhanced ectopic expression of RBM3 using lentiviral-based delivery to the hippocampus, the brain region that is important for memory formation, restored cold-induced synaptic regeneration in the two mouse models of neurodegenerative disease. Moreover, RBM3 overexpression reduced prion neuropathology, prevented neuronal loss, and significantly enhanced the survival of prion-diseased animals. Ectopic RBM3 expression before exposure of young mice with neurodegenerative disease to two consecutive cold-shocks one week apart was sufficient to boost endogenous RBM3 expression in the brain and to achieve synaptic protection.
Although the RBM3-based mechanism of synaptic regeneration remains unknown, these data suggest that RBM3 might have long-term neuroprotective effects. The results of this study could have far-reaching consequences for enhancing cold-shock pathways as a new therapeutic approach for treating neurodegenerative disease.
D. Peretti et al., RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration. Nature 518, 236–239 (2015). [PubMed]

 

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