Researchers halt the progression of spinocerebellar ataxia type 17 in a cell model

Similar to Alzheimer’s disease, the hereditary disease spinocerebellar ataxia type 17 (SCA17) leads to the destruction of brain nerve cells and the premature death of patients. The exact mechanisms of this disease are unknown, which is why there are no treatment approaches as yet. Researchers from the Department of Human Genetics at Ruhr-Universität Bochum headed by Dr. Jonasz Weber now suspect that a class of protein-cleaving enzymes, so-called calpains, may play a role in the disease. By inactivating calpains, the researchers were able to halt the progression of the disease in a cell model. They published a report of their findings in the journal Cellular and Molecular Life Sciences on 28 April 2022.

This article was originally published on MedicalXpress.com

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