Research ArticleNeurodegenerative Disease

Loss of dual leucine zipper kinase signaling is protective in animal models of neurodegenerative disease

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Science Translational Medicine  16 Aug 2017:
Vol. 9, Issue 403, eaag0394
DOI: 10.1126/scitranslmed.aag0394

A new therapeutic target zips into view

The genetics, pathology, and clinical manifestations of chronic neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), are heterogeneous, which has made the development and testing of candidate therapeutics difficult. Here, Le Pichon et al. identify dual leucine zipper kinase (DLK) as a common regulator of neuronal degeneration in mouse models of ALS and Alzheimer’s disease and in human patient postmortem brain tissue. Deletion of DLK or treatment with a DLK inhibitor resulted in neuronal protection and slowing of disease progression after diverse insults in several mouse models of neurodegenerative disease. This suggests that DLK may have broad applicability as a therapeutic target for the treatment of a number of neurodegenerative diseases.

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