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Thread: Turning glial cells into neurons

  1. #1

    Turning glial cells into neurons

    Has anyone else heard of this? The page below, while being a fundraising page, provides more information. It is not directed solely towards SCI but certainly could be a piece of the puzzle.

  2. #2
    I read on that just awhile back and they mentioned trying it on SCI. I thought the open paper yesterday in Nature Communications on motor neurons was very exciting also.

  3. #3
    Senior Member
    Join Date
    Jan 2009
    Baldwinsville, N.Y.
    It would be great if they could fire up some lower moter neurons. I would be happy with that to maybe bring back B & B function.

  4. #4
    At our Summer Open House, July 16: Dr. Paul Lu, Bridging the Injured Spinal Cord with Neural Stem Cells.

  5. #5
    Jim, that's awesome! I can't wait for it now!

  6. #6
    Question 1: Why do you think it was that Dr. Oswald Steward could not replicate the results you had in your 2012 paper?

  7. #7
    Senior Member Moe's Avatar
    Join Date
    Sep 2012
    Thanks Jim, I might drop by to this one, I might spend my vacation in Jersey this year...

  8. #8
    Senior Member
    Join Date
    May 2005
    Very encouraging news

  9. #9
    Nowhere Man, what paper are you referring to regarding Oz Steward not being able to replicate? Wise

  10. #10
    Quote Originally Posted by Wise Young View Post
    Nowhere Man, what paper are you referring to regarding Oz Steward not being able to replicate? Wise

    As part of the NIH "Facilities of Research Excellence-Spinal Cord Injury" project to support independent replication, we repeated key parts of a study reporting robust engraftment of neural stem cells (NSCs) treated with growth factors after complete spinal cord transection in rats. Rats (n=20) received complete transections at thoracic level 3 (T3) and 2weeks later received NSC transplants in a fibrin matrix with a growth factor cocktail using 2 different transplantation methods (with and without removal of scar tissue). Control rats (n=9) received transections only. Hindlimb locomotor function was assessed with the BBB scale. Nine weeks post injury, reticulospinal tract axons were traced in 6 rats by injecting BDA into the reticular formation. Transplants grew to fill the lesion cavity in most rats although grafts made with scar tissue removal had large central cavities. Grafts blended extensively with host tissue obliterating the astroglial boundary at the cut ends, but in most cases there was a well-defined partition within the graft that separated rostral and caudal parts of the graft. In some cases, the partition contained non-neuronal scar tissue. There was extensive outgrowth of GFP labeled axons from the graft, but there was minimal ingrowth of host axons into the graft revealed by tract tracing and immunocytochemistry for 5HT. There were no statistically significant differences between transplant and control groups in the degree of locomotor recovery. Our results confirm the previous report that NSC transplants can fill lesion cavities and robustly extend axons, but reveal that most grafts do not create a continuous bridge of neural tissue between rostral and caudal segments.

    Question 2: What is your plan to prevent tumors from forming after transplantation? Why were they missed in the original study?

    We reported previously the formation of ectopic colonies in widespread areas of the nervous system after transplantation of fetal neural stem cells (NSCs) into spinal cord transection sites. Here, we characterize the incidence, distribution, and cellular composition of the colonies. NSCs harvested from E14 spinal cords from rats that express GFP were treated with a growth factor cocktail and grafted into the site of a complete spinal cord transection. Two months after transplant, spinal cord and brain tissue were analyzed histologically. Ectopic colonies were found at long distances from the transplant in the central canal of the spinal cord, the surface of the brainstem and spinal cord, and in the fourth ventricle. Colonies were present in 50% of the rats, and most rats had multiple colonies. Axons extended from the colonies into the host CNS. Colonies were strongly positive for nestin, a marker for neural precursors, and contained NeuN-positive cells with processes resembling dendrites, GFAP-positive astrocytes, APC/CC1-positive oligodendrocytes, and Ki-67-positive cells, indicating ongoing proliferation. Stereological analyses revealed an estimated 21,818 cells in a colony in the fourth ventricle, of which 1005 (5%) were Ki-67 positive. Immunostaining for synaptic markers (synaptophysin and VGluT-1) revealed large numbers of synaptophysin-positive puncta within the colonies but fewer VGluT-1 puncta. Continuing expansion of NSC-derived cell masses in confined spaces in the spinal cord and brain could produce symptoms attributable to compression of nearby tissue. It remains to be determined whether other cell types with self-renewing potential can also form colonies.

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