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• W2747341145 abstract "Hallmarks of chronic neurodegenerative disease include progressive synaptic loss and neuronal cell death, yet the cellular pathways that underlie these processes remain largely undefined. We provide evidence that dual leucine zipper kinase (DLK) is an essential regulator of the progressive neurodegeneration that occurs in amyotrophic lateral sclerosis and Alzheimer's disease. We demonstrate that DLK/c-Jun N-terminal kinase signaling was increased in mouse models and human patients with these disorders and that genetic deletion of DLK protected against axon degeneration, neuronal loss, and functional decline in vivo. Furthermore, pharmacological inhibition of DLK activity was sufficient to attenuate the neuronal stress response and to provide functional benefit even in the presence of ongoing disease. These findings demonstrate that pathological activation of DLK is a conserved mechanism that regulates neurodegeneration and suggest that DLK inhibition may be a potential approach to treat multiple neurodegenerative diseases." @default.
• W2747341145 created "2017-08-31" @default.
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• W2747341145 date "2017-08-16" @default.
• W2747341145 modified "2023-10-17" @default.
• W2747341145 title "Loss of dual leucine zipper kinase signaling is protective in animal models of neurodegenerative disease" @default.
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• W2747341145 doi "https://doi.org/10.1126/scitranslmed.aag0394" @default.
• W2747341145 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28814543" @default.
• W2747341145 hasPublicationYear "2017" @default.
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