Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Saturday, February 15, 2014

Astroglial-Derived Periostin Promotes Axonal Regeneration after Spinal Cord Injury

Axonal regeneration and sprouting are needed for our recovery. Do your doctors have any idea what it is? Or why it's important to your recovery?
http://www.jneurosci.org/content/34/7/2438.short 
  1. Christoph Pröschel1,2
  1. Author contributions: C.-H.S. and C.P. designed research; C.-H.S., M.L., K.L.-B., and C.P. performed research; C.-H.S. and C.P. analyzed data; C.-H.S. and C.P. wrote the paper.
  1. The Journal of Neuroscience, 34(7): 2438-2443; doi: 10.1523/JNEUROSCI.2947-13.2014

Abstract

Traumatic spinal cord injury (SCI) results in a cascade of tissue responses leading to cell death, axonal degeneration, and glial scar formation, exacerbating the already hostile environment and further inhibiting axon regeneration. Overcoming these inhibitory cues and promoting axonal regeneration is one of the primary targets in developing a cure for SCI. Previously, we demonstrated that transplantation of bone morphogenetic protein (BMP)-induced astrocytes derived from embryonic glial-restricted precursors (GDAsBMP) promotes extensive axonal growth and motor function recovery in a rodent spinal cord injury model. Here, we identify periostin (POSTN), a secreted protein, as a key component of GDABMP-induced axonal regeneration. POSTN is highly expressed by GDAsBMP and the perturbation of POSTN expression by shRNA diminished GDABMP-induced neurite extension in vitro. We also found that recombinant POSTN is sufficient to overcome the inhibitory effect of scar-associated molecules and promote neurite extension in vitro by signaling through focal adhesion kinase and Akt. Furthermore, transplantation of POSTN-deficient GDAsBMP into the injured rat spinal cord resulted in compromised axonal regeneration, indicating that POSTN plays an essential role in GDABMP-mediated axonal regeneration. This finding reveals not only one of the major mechanisms underlying GDABMP-dependent recovery from SCI, but also the potential of POSTN as a therapeutic agent for traumatic injury of the CNS.

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