The study entitled, “Neurological Functional Recovery after Thymosin Beta 4 Treatment in Mice with Experimental Auto Encephalomyelitis,” was published online ahead of print in Neuroscience, 2009 September 24. The publication highlights the statistically significant effects of Tβ4 treatment in EAE mice, including improvement of neurological functional recovery, reduction of inflammatory infiltrates in the brain, and increase of oligodendrocyte progenitor cells (a type of stem cell) and mature oligodendrocytes in the brain.

The research team was led by Jing Zhang, MD, PhD; Zheng Gang Zhang, MD, PhD; Dan Morris, MD; Yi Li, MD; Cynthia Roberts, Stanton B. Elias, MD, and Michael Chopp, PhD of the Departments of Neurology and Emergency Medicine at the Henry Ford Health System in Detroit, Michigan and the Department of Physics at Oakland University in Rochester, Michigan.

Galanin is a protein which, according to Professor David Wynick, has been recognized for some time as offering protection for all of the body’s nerve systems (you can read Wikipedia’s definition of galanin here). Now, in tests conducted on mice by a team brought together by Professor Wynick, it has been established that in high quantities galanin offers complete resistance to Experimental Autoimmune Encephalomyelitis (EAE), a disease introduced in to animals, mainly rodents, by scientists wanting to replicate human MS. Further tests were then conducted on human brain tissue, the nerve cells of the brain contain galanin, and the resistance to MS was confirmed once more. Whilst the results of the tests are certainly welcome, producing a cure for MS, or even a means to reduce its severity will, reports the BBC, still take something like ten years.

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Thursday, 9 April 2009 Wendy Zukerman
ABC

Mice with a human equivalent of multiple sclerosis have been successfully treated using genetically modified stem cells, say a group of Australian researchers.

The work, led by Dr James Chan of Monash University’s Centre of Inflammatory Diseases, may lead to the development of a similar technique to treat autoimmune diseases in humans.

Autoimmune diseases, such as type 1 diabetes and multiple sclerosis, are caused when immune cells, called T cells, incorrectly identify proteins created by the body as foreign objects, such as bacteria, and attack them.

To prevent these rogue T cells from entering the bloodstream, the immune system lures them with ‘self-proteins’ while they are developing in the thymus. T cells that bind tightly to these self-proteins are destroyed by the body’s immune system.

Some slip through this ‘net’ and for some people result in auto-immune disease.

Fully recovered

Chan and colleagues genetically modified a specific type of stem cell, which produce more self-protein to ensure that dangerous T cells are more effectively removed from the system.

In the study, which appeared in the Journal of Immunology, mice were inoculated to develop experimental autoimmune encephalomyelitis (EAE), the human equivalent of multiple sclerosis. The genetically modified stem cells were then transplanted into the mice.

“After the transplantation, the mice are completely resistant to disease,” says Chan.

While initial results are promising, Chan says human clinical trials would not be possible for some time.

“Before we transplant the stem cells we wipe out the immune system of the mice using high doses irradiation,” says Chan.

He says this level of irradiation would not suitable for humans.

The team is now looking at ways of overcoming the need for radiation, in order to make the procedure clinically viable.

Promising

Dr Carola Vinuesa of the John Curtin School of Medical Research at the Australian National University in Canberra, says the results are “very exciting and potentially very promising.”

But Vinuesa cautions that it is unclear how well the mouse model relates to human disease.

“The EAE mouse model of multiple sclerosis is not a model in which autoimmune disease develops spontaneously, as occurs with multiple sclerosis in humans,” she says.

She adds there is still a lot we don’t know about how healthy T cells know not to attack self-proteins.

“The mechanism by which they do this is still unclear, but the results [from this study] are spectacular,” says Vinuesa.

View entire post here: http://www.abc.net.au/science/articles/2009/04/09/2539614.htm?site=science&topic=latest