Fri, Aug 10, 2007 - Page 2 News List

Study may help brain disorders

PROMISING TREATMENT A researcher said that if successful, G-CSF therapy could open up a new avenue of Alzheimer's treatment that is less invasive and more effective

By Angelica Oung  /  STAFF REPORTER

A team of scientists from the National Science Council have found that a human growth factor that triggers the release of stem cells from bone marrow shows potential as a treatment for Alzheimer's disease and other degenerative brain disorders.

Shen Che-kun (沈哲鯤), a researcher at Academia Sinica's institute of molecular biology, told a press conference yesterday that the team's studies showed that Granulocyte-colony stimulating factor (G-CSF) appeared to reverse Alzheimer's-like symptoms in AD mouse models.

This is the first piece of research that applies G-CSF therapy, most often used to accelerate recovery from chemotherapy, to Alzheimer's disease, he said.

"Studies conducted on mice show that G-CSF not only arrests deterioration in mental capacity but allows the affected mice to recover lost mental capacity to levels comparable to normal mice of the same age," Shen said.

The team used two AD mouse models with Alzheimer's dislike symptoms -- one was generated by injecting the brains of normal mice with beta-amyloid protein and another was a strain of transgenic mice which naturally exhibit Alzheimer's disease-like neuronal apoptosis and memory loss.

The study, co-authored by Shen and Tsai Kuen-jer (蔡坤哲), also of the institute of molecular biology, was published in the June issue of the Journal of Experimental Medicine.

G-CSF is a growth factor that is naturally present in the body in small quantities and is thought to be linked with the regeneration of brain tissue, Shen said.

During their study, researchers injected G-CSF directly into the mice's thorax. Its presence in the bloodstream facilitated the release of hematopoietic stem cells from bone marrows, Shen said.

Although Shen and Tsai said that they have not conclusively proved the mechanism by which the damage was repaired, Shen said that he thought it was most likely that the stem cells released by the G-CSF injection from the bone marrow passed into the brain from the bloodstream, where they attached to sites of damage and became differentiated into new cells.

"There have been previous studies where injections of G-CSF into the bloodstream was found to repair damaged heart tissue," Shen said. "In our case, we saw that the G-CSF injection appeared to cause new cells to grow where the neuron damage was the greatest."

If successful, G-CSF therapy could open up a new avenue of Alzheimer's treatment that is less invasive and more effective than current therapies, Shen said.

"However, remember that it has only been found effective in mice so far," cautioned Shen, who said that further trials on human subjects were needed to determine the treatment's efficacy and safety.

If the drug proves to be effective in clinical testing, it may become available on the market in as little as five years, the researchers said.

Because G-CSF is already widely used to treat neutropenia in chemotherapy patients, the drug does not have to undergo pre-clinical toxicological testing or phase I clinical testing.

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