Author

Christopher Patzke

University of Notre DameORCID 0000-0001-7293-8936Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Organism:mouse· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

Anna WenningeriD· 2 shared Cameron MacKenzie· 2 shared Charles SanderiD· 2 shared Jenny Bergqvist-PatzkeiD· 2 shared Alan Michael PittmaniD· 1 shared Alexander Weaver· 1 shared Alexandra NobleiD· 1 shared Alice A. BurchettiD· 1 shared

Activity by Year

2021-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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2 shared papersNeuroscience

Anna WenningerORCID

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Author profile →

3 papers

Recent·Most cited

Mechanical compression induces neuronal apoptosis, reduces synaptic activity, and promotes glial neuroinflammation in mice and humans

Maksym Zarodniuk, Anna Wenninger, Julian Najera, Jihaeng Lee, Jack Markillie, Cameron MacKenzie, Jenny Bergqvist-Patzke, Bianca Batista, Megna A. Panchbhavi, R’nld Rumbach, Alice A. Burchett, Charles Sander, Meenal Datta, Christopher Patzke

The paper shows mechanical compression causes neuronal apoptosis, synaptic loss, and glial inflammation in GBM models, revealing pathways for neuroprotection.

Proceedings of the National Academy of Sciences · Jan 2, 2026Peer-reviewedNeuroscience

Human Neuron and Mouse Models Reveal Synaptic Imbalance in Kabuki Syndrome

Anna Wenninger, James Knopp, Steven Frye, Alexander Weaver, Neil McAdams, Sean Miller, Toshihiro Nomura, Ava Whitlark, Jack Swantkowski, Alexandra Noble, Caroline Lavender, Sandy Nam, Cameron MacKenzie, Isabella Wiebelt-Smith, Charles Sander, , Christopher Patzke

This study uses human and mouse models to show that Kabuki syndrome mutations cause an imbalance in excitatory and inhibitory synapses, leading to synaptic dysfunction and intellectual disability.

bioRxiv · Oct 4, 2024 · PreprintNeuroscience

Bi-allelic variants in TSPOAP1, encoding the active zone protein RIMBP1, cause autosomal recessive dystonia

Niccolò Emanuele Mencacci, Marisa M. Brockmann, Jinye Dai, Sander Pajusalu, Burcu Atasu, Paulina González-Latapí, Christopher Patzke, Michael Schwake, Arianna Tucci, Alan Michael Pittman, Javier Simón‐Sánchez, Gemma L. Carvill, Bettina Balint, Sarah Wiethoff, Thomas T. Warner, , Claudio Acuna

The paper identifies bi-allelic variants in TSPOAP1 as a cause of autosomal recessive dystonia, showing different clinical presentations based on variant type.

Journal of Clinical Investigation · Feb 4, 2021Peer-reviewedGenetics