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West Ashley Library
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Folly Beach Library
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Wando Mount Pleasant Library
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Multiomic ALS signatures highlight subclusters and sex differences suggesting the MAPK pathway as therapeutic target.
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- Author(s): Caldi Gomes, Lucas; Hänzelmann, Sonja; Hausmann, Fabian; Khatri, Robin; Oller, Sergio; Parvaz, Mojan; Tzeplaeff, Laura; Pasetto, Laura; Gebelin, Marie; Ebbing, Melanie; Holzapfel, Constantin; Columbro, Stefano Fabrizio; Scozzari, Serena; Knöferle, Johanna; Cordts, Isabell; Demleitner, Antonia F.; Deschauer, Marcus; Dufke, Claudia; Sturm, Marc; Zhou, Qihui
- Source:
Nature Communications; 6/7/2024, Vol. 15 Issue 1, p1-23, 23p- Subject Terms:
- Source:
- Additional Information
- Abstract: Amyotrophic lateral sclerosis (ALS) is a debilitating motor neuron disease and lacks effective disease-modifying treatments. This study utilizes a comprehensive multiomic approach to investigate the early and sex-specific molecular mechanisms underlying ALS. By analyzing the prefrontal cortex of 51 patients with sporadic ALS and 50 control subjects, alongside four transgenic mouse models (C9orf72-, SOD1-, TDP-43-, and FUS-ALS), we have uncovered significant molecular alterations associated with the disease. Here, we show that males exhibit more pronounced changes in molecular pathways compared to females. Our integrated analysis of transcriptomes, (phospho)proteomes, and miRNAomes also identified distinct ALS subclusters in humans, characterized by variations in immune response, extracellular matrix composition, mitochondrial function, and RNA processing. The molecular signatures of human subclusters were reflected in specific mouse models. Our study highlighted the mitogen-activated protein kinase (MAPK) pathway as an early disease mechanism. We further demonstrate that trametinib, a MAPK inhibitor, has potential therapeutic benefits in vitro and in vivo, particularly in females, suggesting a direction for developing targeted ALS treatments. Multiomic brain tissue analysis identified sex-specific molecular changes in Amyotrophic lateral sclerosis (ALS), revealing subgroups within the disease and pointing to the MAPK pathway as an early disease mechanism and potential therapeutic target. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Nature Communications is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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