Researchers Report In Neuroscience That TB4 Improves Neurological Function After Stroke

Main Category: Neurology / Neuroscience
Also Included In: Stroke
Article Date: 21 Jul 2010 - 0:00 PDT

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RegeneRx Biopharmaceuticals, Inc. (NYSE Amex:RGN) ("the Company" or "RegeneRx") announced a research team from the Henry Ford Hospital in Detroit, MI, reported that Thymosin beta 4 (Tβ4), administered to rats after embolic stroke, improved neurological functional outcome compared to control animals.

The research was conducted by Dr. Daniel Morris and his colleagues at the Department of Emergency Medicine, Henry Ford Health System, Detroit, MI, and published in Neuroscience, 2010 Aug 25 169(2) 674-682, see here. The research was performed under a Material Transfer Agreement between RegeneRx Biopharmaceuticals, Inc. and the Henry Ford Health System.

Improvement in neurological function was measured at various time intervals over a seven week period and was statistically significant. A statistically significant increase in remyelination of axons and vessel density in the ischemic boundary was also observed between rats receiving Tβ4 vs. controls, likely due to an increased mobilization of oligodendrocyte progenitor cells (brain stem cells that differentiate into cells that protect nerve fibers). mRNA levels for the epidermal growth factor receptor were determined in both normal and stroke rats treated with Tβ4 and were approximately 50% higher in the stroke-treated rats. This receptor has previously been shown to be a key regulator of progenitor cell expansion and tissue regeneration in response to brain injury and further confirms the role of Tβ4 in stem cell-mediated tissue repair.

"Some of these data were previously reported at an International Stroke Conference in March; however, the data published today include more specific information on functional remodeling and potential mechanisms of action related to recruitment and differentiation of oligodendrocyte progenitor cells. These data are compelling and elaborate previously reported data in EAE mice (experimental models for multiple sclerosis) and in traumatic brain injury in rats showing that Tβ4 can effect regeneration of neuronal cells after injury. In this experiment, after an ischemic stroke, neurological function in the rat models was significantly improved, apparently by remyelination of neurological axons (nerve fibers that conduct electrical signals) induced by Tβ4. The fact that Tβ4 helps repair and regenerate tissue after a brain injury strongly correlates with other published data showing Tβ4's ability to regenerate neuronal and cardiac tissue after ischemic events," stated Dr. Hynda Kleinman, former head of cell biology at the National Institute of Dental and Craniofacial Research, NIH, and a consultant to RegeneRx.

About Tβ4

Tβ4 is a synthetic version of a naturally occurring peptide present in virtually all human cells. It is a first-in-class multi-functional molecule that has been shown in pre-clinical studies to promote endothelial cell differentiation and migration in the heart and central nervous system, promote angiogenesis in dermal and cardiac tissues, increase keratinocyte migration and collagen deposition, and decrease inflammation by down-regulating inflammatory cytokines. RegeneRx has identified several molecular variations of Tβ4 that may affect the aging of skin, among other properties, and could be important candidates as active ingredients in pharmaceutical and consumer products. Researchers at the National Institutes of Health and various academic researchers throughout the world have published numerous scientific articles in high impact journals indicating Tβ4's in vitro and in vivo efficacy in accelerating wound healing and tissue protection and regeneration under a variety of conditions.

Source:
RegeneRx Biopharmaceuticals, Inc.

Article adapted by Medical News Today from original press release.
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RegeneRx Biopharmaceuticals, Inc.. "Researchers Report In Neuroscience That TB4 Improves Neurological Function After Stroke." Medical News Today. MediLexicon, Intl., 21 Jul. 2010. Web.
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