Author

Zoe N. Burch

Massachusetts General Hospital

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Genetics· 2 Neuroscience· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:mouse· 4 Research Focus:benchmarking· 1 Research Focus:drug response / drug discovery· 1 Organism:human· 1 Approach:statistical model· 1

Frequent Co-Authors

Vanessa Chantal WheeleriD· 4 shared Marina V. KovalenkoiD· 3 shared Ricardo Mouro PintoiD· 3 shared Antonia G. Vitalo· 2 shared Eduarda Mota‐SilvaiD· 2 shared Jeffrey B. CarrolliD· 2 shared Marissa A Andrew· 2 shared Alyssa SolesiD· 1 shared

Activity by Year

2021-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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4 shared papersNeuroscience

Vanessa Chantal WheelerORCID

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Author profile →

4 papers

Recent·Most cited

Suppression of Huntington's Disease Somatic Instability by Transcriptional Repression and Direct CAG Repeat Binding

Ella W. Mathews, Sydney R. Coffey, Annette Gärtner, Jillian Belgrad, Robert M. Bragg, Daniel O’Reilly, Jeffrey P. Cantle, Cassandra A. McHugh, Ashley Summers, Joachim Fentz, Tom Schwagarus, Antje Cornelius, Ioannis Lingos, Zoe N. Burch, Marina V. Kovalenko, , Jeffrey B. Carroll

This study investigates how different HTT-lowering therapies affect somatic instability in HD mice, finding that transcriptional repression and CAG repeat binding reduce SI without lowering HTT levels.

Nature Communications · Nov 14, 2025Peer-reviewedNeuroscience

Identification of genetic modifiers of Huntington's disease somatic CAG repeat instability by in vivo CRISPR-Cas9 genome editing

Ricardo Mouro Pinto, Ryan Murtha, António Azevedo, Cameron J. Douglas, Marina V. Kovalenko, Jessica Ulloa, Steven Crescenti, Zoe N. Burch, Esaria Oliver, Maheswaran Kesavan, Shota Shibata, Antonia G. Vitalo, Eduarda Mota‐Silva, Marion J. Riggs, Kevin Correia, , Vanessa Chantal Wheeler

The paper identifies genetic modifiers of Huntington's disease somatic CAG repeat instability using CRISPR-Cas9 in HD knock-in mice, revealing new therapeutic targets.

Nature Genetics · Jan 22, 2025Peer-reviewedGenetics

Delineating regional vulnerability in the neurodegenerative disease SCA1 using a conditional mutant ATXN1 mouse

Lisa A. Duvick, William M. Southern, Kellie A. Benzow, Zoe N. Burch, Hillary P. Handler, Jason S. Mitchell, Hannah Kuivinen, Udaya Keerthy Gadiparthi, Praseuth Yang, Alyssa Soles, Carrie A. Sheeler, Orion Rainwater, Shannah Serres, Erin B. Lind, Tessa Nichols‐Meade, , Harry T. Orr

This study identifies brain regions and cell types contributing to SCA1 disease using conditional knockout mice, showing that targeting multiple areas and muscle is necessary for effective therapy.

bioRxiv · Feb 8, 2023 · PreprintNeuroscience

Somatic CAG expansion in Huntington's disease is dependent on the MLH3 endonuclease domain, which can be excluded via MLH3 splice redirection to suppress expansion

Jennie C. L. Roy, Antonia G. Vitalo, Marissa A Andrew, Eduarda Mota‐Silva, Marina V. Kovalenko, Zoe N. Burch, Anh M. Nhu, Paula E. Cohen, Ed Grabczyk, Vanessa Chantal Wheeler, Ricardo Mouro Pinto

This study shows that targeting the MLH3 endonuclease domain reduces somatic CAG expansion in Huntington's disease models and patient cells.

Nucleic Acids Research · Feb 23, 2021Peer-reviewedGenetics