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.

Monday, July 1, 2019

Nogo-A targeted therapy promotes vascular repair and functional recovery following stroke

Some earlier research goes back to 2001 so we have had failures at the highest levels for decades in stroke leadership in not following up promising stroke rehab and recovery.  Firings should have commenced decades ago.

  • nogo (7 posts to January 2012)

  • nogo-A (9 posts back to May 2012)

 

Nogo-A targeted therapy promotes vascular repair and functional recovery following stroke

Ruslan Rust, Lisa Grönnert, Christina Gantner, Alinda Enzler, Geertje Mulders, Rebecca Z. Weber, Arthur Siewert, Yanuar D. P. Limasale, Andrea Meinhardt, Michael A. Maurer, Andrea M. Sartori, Anna-Sophie Hofer, Carsten Werner, and Martin E. Schwab
  1. Edited by Michael E. Greenberg, Harvard Medical School, Boston, MA, and approved May 31, 2019 (received for review March 28, 2019)

Significance

Patients suffering from ischemic strokes have limited therapeutic options and are often left with considerable disabilities. To promote neurological recovery, angiogenesis has been proposed as a promising therapeutic target. So far, experimental efforts to enhance vessel growth have almost exclusively focused on vascular growth factor supplementation; this approach has been shown not to be clinically viable due to hemorrhagic risks. Here, we pursued an alternative approach by targeting the guidance molecule Nogo-A, which has been recently shown to inhibit developmental central nervous system angiogenesis. Blockage of the Nogo-A pathway results in restoration of a mature vascular bed within the periinfarct zone. Moreover, we observe enhanced recovery-associated tissue responses and regain of motor functions that strongly correlate with vascular growth.

Abstract

Stroke is a major cause of serious disability due to the brain’s limited capacity to regenerate damaged tissue and neuronal circuits. After ischemic injury, a multiphasic degenerative and inflammatory response is coupled with severely restricted vascular and neuronal repair, resulting in permanent functional deficits. Although clinical evidence indicates that revascularization of the ischemic brain regions is crucial for functional recovery, no therapeutics that promote angiogenesis after cerebral stroke are currently available. Besides vascular growth factors, guidance molecules have been identified to regulate aspects of angiogenesis in the central nervous system (CNS) and may provide targets for therapeutic angiogenesis. In this study, we demonstrate that genetic deletion of the neurite outgrowth inhibitor Nogo-A or one of its corresponding receptors, S1PR2, improves vascular sprouting and repair and reduces neurological deficits after cerebral ischemia in mice. These findings were reproduced in a therapeutic approach using intrathecal anti–Nogo-A antibodies; such a therapy is currently in clinical testing for spinal cord injury. These results provide a basis for a therapeutic blockage of inhibitory guidance molecules to improve vascular and neural repair after ischemic CNS injuries.

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