![]() ![]() The existence of common mechanisms of neurodegeneration has long been hypothesized. The DLK-dependent injury response promotes neurodegeneration in the mammalian CNS. The lab is currently investigating how such diverse diseases converge upon this single pathway and how this pathway mediates divergent fates. We showed that Dual Leucine Zipper Kinase (DLK MAP3K12) acts as a crucial downstream node in neurodegeneration and neuropathy, two pathologies with very different causes and outcomes (Le Pichon et al., 2017 Wlaschin et al., 2018). An understanding of any common mechanisms involved in neurodegeneration would provide major breakthroughs for designing treatments. The vast majority of cases have no established genetic etiology and therefore no clear pathway to target. However, the linkages only account for a relatively small proportion of all cases. Most of what is currently understood about neurodegenerative disease stems from the identification of genetic linkages that are causative or predisposing, and from efforts to uncover the mechanisms underlying these linkages. The hypothesis driving our work is that common mechanisms are responsible for neurodegeneration during development, childhood, and aging. ![]() As a cellular stress response pathway in neurons, its function is to promote recovery from injury however, at the same time, it can drive several types of pathologies, including peripheral neuropathies and neurodegeneration. The lab currently focuses on investigating an evolutionarily conserved neuronal stress response pathway under control of DLK (dual leucine zipper kinase), which plays an important role in several neuropathologies. Our work is dedicated to the better understanding of common molecular and cellular mechanisms of neurodegeneration, with the ultimate goal of developing treatments for neurodegenerative diseases and even preventing them. ![]()
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