A new study led by Amorfix Life Sciences’ Chief Scientific Officer Dr. Neil Cashman and published February 18 online in Proceedings of the National Academy of Sciences, sheds light on how ALS spreads throughout the nervous system. The researchers have previously shown that mutant SOD1 can cause wild-type SOD1 to misfold and acquire toxic properties. This new report shows that misfolded SOD1 can also spread from cell to cell, and induce template-directed misfolding of native SOD1 via a prion-like mechanism. Prion-like proteins are not new to ALS – TDP-43 also exhibits prion-like properties. These findings provide additional research support for Amorfix’s approach to treating ALS by developing therapeutic antibodies that target misfolded SOD1.
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