ALS Research Roundup October 2007

by Margaret Wahl on Mon, 2007-10-01 09:16
Article Highlights:

Research updates as of September 2007:

Emotional-control drug development to move forward, Avanir says

The experimental drug Zenvia is designed to control involuntary laughing and crying.

Avanir Pharmaceuticals of Aliso Viejo, Calif., has announced that it will continue developing Zenvia (formerly called Neurodex), a medication designed to control involuntary emotional expression (laughing and/or crying) in ALS and other neurologic disorders. The current Zenvia trial is no longer recruiting participants.

In an Aug. 6 press release, the company announced that it had completed the sale of its antipsychotic drug FazaClo (clozapine) and that it expects the income from this sale and other revenue sources “will be sufficient to finance operating expenses through the end of the next fiscal year, including the initiation of the planned confirmatory phase III clinical trial of Zenvia in patients with involuntary expression disorder (IEED), otherwise known as pseudobulbar affect (PBA).”

Human stem cells secreting GDNF protected dying motor neurons

Last month, scientists at the University of Wisconsin-Madison and in Lausanne, Switzerland, announced they had protected motor neurons in ALS-affected rats by transplanting human stem cells modified to secrete a therapeutic protein into their spinal cords. Motor neurons are the muscle-controlling nerve cells affected in ALS.

Masatoshi Suzuki and colleagues, who published their results Aug. 1 in the Public Library of Science online journal PLoS One, inserted genes for glial-derived neurotrophic factor (GDNF), a protein known to protect nerve cells, into cells derived from fetal brain tissue under National Institutes of Health guidelines. They then injected the cells into one side of each rat’s spinal cord. Six weeks later, the side that didn’t get the stem cells showed a 70 percent reduction in motor neuron cell number, while the stem-cell-injected side showed almost no loss of motor neurons.

Unfortunately, however, the surviving neurons did not appear to maintain their normal contacts with muscle fibers, and the rats experienced no functional improvement.

“While these results are encouraging, challenges remain,” said Valerie Cwik, MDA’s medical director and vice president of research. “Future research strategies will need to address this issue.”

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Margaret Wahl
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