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Researchers identify new genetic defect linked to ALS

Mutations in the UBQLN2 gene, known to cause amyotrophic lateral sclerosis (ALS), promote the buildup of toxic waste in brain cells by preventing the normal function of two cellular degradation mechanisms, a study has found.

In addition to its known role in the proteasome, a mechanism used for clearing out abnormal proteins, the UBQLN2 protein also is needed for autophagy, another recycling mechanism used to eliminate larger components of cells, including the toxic protein aggregates seen in ALS patients.

The study, “ALS/FTD mutations in UBQLN2 impede autophagy by reducing autophagosome acidification through loss of function,” was published in PNAS.

Oxford Biodynamics PLC (LON:OBD) was spun out from Oxford University in June 2007 with the aim of translating fundamental scientific advances into a commercialised platform technology and a new generation of biomarkers for cancer, ALS and other diseases.

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