Author

Michael H. Brodsky

University of Massachusetts Chan Medical SchoolORCID 0000-0001-7703-4872Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Molecular Biology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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Organism:mouse· 2 Assay:bulk RNA-seq· 1 Assay:CRISPR screen· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1

Frequent Co-Authors

Robert H. BrowniD· 2 shared Abbas Abdallah· 1 shared Alexander JaworskiiD· 1 shared Alexandra Weiss· 1 shared Alireza EdrakiiD· 1 shared Alper KüçükuraliD· 1 shared Aydan KahrimaniD· 1 shared Carolyn KrausiD· 1 shared

Activity by Year

2022-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersNeuroscience

Robert H. BrownORCID

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2 papers

Recent·Most cited

NeurosciencebioRxivPreprintMay 5, 2023

Up-regulation of cholesterol synthesis pathways and limited neurodegeneration in a knock-in Sod1 mutant mouse model of ALS.

Janice A. Dominov, Laura A. Madigan, Joshua P. Whitt…·Robert H. Brown

This study shows that Sod1G85R knock-in mice exhibit up-regulated cholesterol synthesis pathways and limited neurodegeneration, contrasting with severe TgSOD1G93A mice, suggesting lipid pathway dysregulation in ALS.

7 citations

mousebulk RNA-seq

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Molecular BiologyNature CommunicationsPeer-reviewedOct 21, 2022

CRISPR/Cas9-Mediated Excision of ALS/FTD-Causing Hexanucleotide Repeat Expansion in C9ORF72 rescues major disease mechanisms in vivo and in vitro

Katharina E. Meijboom, Abbas Abdallah, Nicholas P. Fordham…·Christian Mueller

This study removes a hexanucleotide repeat expansion in C9ORF72 using CRISPR/Cas9 in cell and animal models, reducing disease hallmarks.

72 citationstop 2%

mousehuman

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