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New model of ALS is based on human cells from autopsied tissue
Date:8/11/2011

n overnight, the Columbus team was able to process the samples in the current study within two to three days of death.

First, the researchers isolated neural progenitor cells from the tissue and coaxed these cells to become astrocytes. Neural progenitor cells are the parent lineage of neurons and astrocytes. Next, the team combined the patient-derived astrocytes with mouse motor neurons. At first, the motor neurons grew normally, but after four days, they began to degenerate. By five days, the number of motor neurons was reduced by about half, compared to motor neurons that had been grown with control astrocytes. Similar results were seen when the motor neurons were grown with astrocytes from a patient with familial ALS, or with a cell culture broth that had been conditioned by astrocytes from any of the ALS patients. This suggests the astrocytes are releasing one or more unknown substances that are toxic to motor neurons.

The researchers found that inflammatory responses may play a role in this toxicity. They analyzed 84 genes involved in inflammation, and found that 35-60 percent of the genes showed increased activity in ALS astrocytes compared to controls.

Further experiments revealed that the SOD1 plays a critical role in the toxicity. The investigators used a method called RNA interference to silence the SOD1 gene. RNA serves as an intermediary between genes and proteins, but in RNA interference, small RNA fragments are used to block a gene from making proteins. When the researchers used a virus to deliver such small RNAs to astrocytes affected by familial ALS, the astrocytes were no longer toxic to motor neurons. This method also suppressed toxicity in four of six astrocyte lines derived from people with sporadic ALS, supporting the idea that the SOD1 enzyme also has a role in sporadic cases.

The results also suggest the need for further investigation of SOD1 and astrocytes as targets for therapy. For example, dr
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Contact: Daniel Stimson
stimsond@ninds.nih.gov
301-496-5751
NIH/National Institute of Neurological Disorders and Stroke
Source:Eurekalert

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