Amyotrophic lateral sclerosis (ALS) is a progressing neurodegenerative disorder. This study validates ALS treatment targets derived from MAXOMOD consortium research. Multiomic analysis of human postmortem prefrontal cortex and ALS mouse models identified XPO1 and MAP2K2 for in vitro validation. Using toxin models, we modulated XPO1 and MAP2K2 expression with FDA-approved inhibitors. Trametinib reduced cell death and enhanced neurite outgrowth, while selinexor mitigated cell death in glutamate-intoxicated and stress granule-induced cells.
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Amyotrophic lateral sclerosis (ALS) is a progressing neurodegenerative disorder. This study validates ALS treatment targets derived from MAXOMOD consortium research. Multiomic analysis of human postmortem prefrontal cortex and ALS mouse models identified XPO1 and MAP2K2 for in vitro validation. Using toxin models, we modulated XPO1 and MAP2K2 expression with FDA-approved inhibitors. Trametinib reduced cell death and enhanced neurite outgrowth, while selinexor mitigated cell death in glutamate-in...
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