Thymosin Beta 4 neuroprotective

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cypress

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PALS
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08/2012
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Do any of you have knowledge or experience with TB4, it is available. RegenRx is testing it

Neuroprotective effects of thymosin beta4 in experimental models of excitotoxicity.

Patrizia Popoli, Rita Pepponi, Alberto Martire, Monica Armida, Antonella Pèzzola, Mariangela Galluzzo, M Rosaria Domenici, Rosa Luisa Potenza, M Teresa Tebano, Cristiana Mollinari, Daniela Merlo, Enrico Garaci
Istituto Superiore di Sanità, Viale Regina Elena, 299 Rome, Italy.
Annals of the New York Academy of Sciences (impact factor: 3.15). 10/2007; 1112:219-24. DOI:10.1196/annals.1415.033
Source: PubMed
ABSTRACT The aim of this study was to evaluate the possible neuroprotective effects of thymosin beta(4) in different models of excitotoxicity. The application of thymosin beta(4) significantly attenuated glutamate-induced toxicity both in primary cultures of cortical neurons and in rat hippocampal slices. In in vivo experiments, the intracerebroventricular administration of thymosin beta(4) significantly reduced hippocampal neuronal loss induced by kainic acid. These results show that thymosin beta(4) induced a protective effect in models of excitotoxicity. The mechanisms underlying such an effect, as well as the real neuroprotective potential of thymosin beta(4), are worthy of further investigations.
 
Lots of views, but no opinions?:sad::sad::sad::sad:
 
Hello cypress,

I read a similar study discussing R1 (risolvin), also done in Italy, but I don't understand much of what I am reading (I'm not a scientist). My wife, however, is a scientist, and she was not all that impressed with the study that I read, saying that it was done in too small an area with too few people, most of whom were related in some way (too many genetic factors possibly involved)......, couldn't be used as "gospel" just yet.

The TB4 study is completely different, but any new info (about any part of this disease) may turn into something significant.......everything is worth a try, in my opinion.

UCLA and Harvard are two places working hard on ALS right now. Maybe you can access some of their findings.....if you understand what you are reading, or can get it explained to you.

Keep searching.....we all are.
 
I can't get very excited about any drug trials. Too disappointing so far.
 
Hello cypress,

I read a similar study discussing R1 (risolvin), also done in Italy, but I don't understand much of what I am reading (I'm not a scientist). My wife, however, is a scientist, and she was not all that impressed with the study that I read, saying that it was done in too small an area with too few people, most of whom were related in some way (too many genetic factors possibly involved)......, couldn't be used as "gospel" just yet.

The TB4 study is completely different, but any new info (about any part of this disease) may turn into something significant.......everything is worth a try, in my opinion.

UCLA and Harvard are two places working hard on ALS right now. Maybe you can access some of their findings.....if you understand what you are reading, or can get it explained to you.

Keep searching.....we all are.
I am starting to dig harder.....there seem to be many things out there that can help. They just don't. I am not a scientist but I am trainable and circumstances make learning a necessity in this case. Unless I can find some direct evidence against trying it out, I am going to. Along with some other Ppary agonists. Maybe some synergy will help. Going down either way, might as well keep punching while I pray.
 
Hang in there, one hour might make a difference.
 
may i recommend "Institute for erthnomedicine.com" Read sections and look over list of articles dating back to 2002. learned today there is still research going on in this area. hope so and wish there was more publicity whats going on in the enviromental area.
 
TB4 is active in Oligodendrocyte differentiation an preservation.
This from ALS/TDI
The oligodendrocyte, a new player in ALS?
Posted by Michelle Pflumm, Ph.D.

July 19, 2012




Insular Messaging. Oligodendrocytes ensure that messages are delivered by neurons quickly and efficiently by insulating (myelinating) them. Adapted from Aubourg, P. (2007), Nature Genetics. Courtesy of Nature Publishing Group. All rights reserved.

In people with ALS, the motor nerves deteriorate leading to muscle weakness and paralysis. Astrocytes and microglia, entrusted to support and protect these cells, turn traitor spewing out neurotoxic cytokines, contributing to disease progression.

ALS, however, is fueled by much more than a perfect storm of neurotoxic substances. Motor neurons face an energy crisis. And, scientists suspect, are without a plan B. Oligodendrocytes, which may help keep the power on in motor neurons, are also disappearing over the course of the disease.

Now, researchers from Johns Hopkins University School of Medicine led by neurologist Jeff Rothstein MD PhD report that oligodendrocytes appear to be the main supplier of energy-rich lactate to nerve cells. And, cutting off the supply of this critical metabolite may lead to neurodegenerative disease.

These results add to growing evidence that the loss of oligodendrocytes in the brain and spinal cord may contribute to the onset and progression of ALS.

The results are published online this month in the journal Nature.




Power hungry. Scientists found that ALS-ravaged motor cortex (a) expresses less than half the level of lactate exporters MCT1 and MCT4 than unaffected regions of the brain (b) in people with ALS suggesting that an interruption in the supply chain might contribute to the disease. Image: Lee, Y. et al. (2012), Nature. Courtesy of Nature Publishing Group.All rights reserved.

The Johns Hopkins University School of Medicine team found that the principal lactate transporter, MCT1, is primarily produced by oligodendrocytes. And, in people with ALS, this delivery vehicle appears to be expressed over 50% less in disease-ravaged regions of the brain.

Together, these findings suggest that reduced delivery of energy-rich lactate by oligodendrocytes may contribute to ALS.

To put this theory to the test, the researchers disrupted the delivery of this energy-rich metabolite via injecting oligodendrocyte-specific MCT1 RNA-interfering lentiviruses in the mouse spinal cord. The team found that more than 50% of motor neurons near the injection site degenerated.

The results come just three months after a Max Planck Institute of Experimental Medicine team led by neuroscientist Klaus Armin-Nave PhD reported that oligodendrocytes may switch to lactate-producing mode to help neurons in energy need.

Looking ahead, these studies suggest that treatments which boost numbers of oligodendrocytes which can deliver this critical energy-rich metabolite may slow the progression of the disease.

To learn more about the emerging role of oligodendrocytes in ALS, check out Jeff Rothstein’s talk at the 2011 ALS TDI Summit. To find out about approaches scientists are exploring to increase oligodendrocyte populations, read our recent feature, Exercise: stretching the limits of ALS care.

References

Fünfschilling, U. et al. (2012) Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity. Nature 485, 517-521. Abstract | Full Text

Kang, S.H., Fukaya, M., Yang, J.K., Rothstein, J.D. and Bergles DE. (2010) NG2+ CNS glial progenitors remain committed to the oligodendrocyte lineage in postnatal life and following neurodegeneration. Neuron 68(4), 668-681. Abstract | Full Text

Lee, Y. et al. (2012) Oligodendroglia metabolically support axons and contribute to neurodegeneration. Nature, doi:10.1038/nature11314. Abstract | Full Text

Further Reading

Nave, K.A. (2010) Myelination and the trophic support of long axons. Nature Reviews Neuroscience 11(4), 275-283. Abstract | Full Text
 
TB4 encourages oligodendrocyte production...just found this today

Researcher Reports That RegeneRx's Thymosin Beta 4 Can Trigger Maturation Of Brain Stem Cells

02 Jun 2011

RegeneRx Biopharmaceuticals, Inc. (OTC Bulletin Board: RGRX) ("the Company" or "RegeneRx") has announced that researchers have found that Thymosin beta 4 (Tβ4), in a dose dependent manner, stimulates oligodendrogenesis, the process by which central nervous system (CNS) progenitor cells (immature specialized brain cells) become oligodendrocytes that secrete myelin, the covering of nerve fibers. This process is important for the repair, regeneration and function of CNS tissue damaged by disease or trauma.

The research team was led by Dr. Dan Morris, of the Henry Ford Hospital System in Detroit, Michigan. Dr. Morris is presenting his findings at the Society of Academic Emergency Medicine meeting on June 1st.

Dr. Morris has previously shown that Tβ4 significantly improves neurological functional outcome in a CNS rat model after embolic stroke. His work in the field brings us closer to understanding the mechanisms underlying the differentiation of immature oligodendrocytes into mature oligodendrocytes in patients suffering stroke, multiple sclerosis and traumatic brain injury.
 
Started on it today, hope it works for all our sakes.
 
Survived day one, no issues.
 
Second dose tonight. Going well, hands seem stronger, definitely steadier. But remember, that is with three supplements .
 
Second dose and all is well. Subject shows improvement in strength and steadiness of weakest limb and overall increase in well being.
 
I've got nothing useful to contribute at this point, but want to encourage you to be persistent and systematic in your search, and keep reporting!
 
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