Ben-Gurion University campus. Photo: Yehudit Garinkol.

JNS.org — A new study published by researchers from Ben-Gurion University (BGU) in the Negev explores a molecular mechanism that could help develop new treatments for ALS, also known as Lou Gehrig’s disease.

Published online in Proceedings of the National Academy of Sciences of the United States of America (PNAS), the study done on mice found that a gene regulating cell inflammation and immunity acts as a chaperone to the misfolded protein that causes the death of motor neurons found in 20 percent of genetic ALS cases. When the researchers eliminated this gene, they found the accumulation of the protein increased and the disease accelerated.

“This study provides insight into the potential therapeutic role” of the studied gene, said Dr. Adrian Israelson, head of the cellular and molecular neurodegeneration lab in the BGU Department of Physiology and Cell Biology.

“Correct protein folding is critically important, which is why we are focusing on the diverse set of complex cellular mechanisms, including molecular chaperones, that promote efficient folding and prevent toxicity,” Israelson said.

ALS is a fatal neurodegenerative disease that destroys motor neurons which control voluntary movement of the muscles.