Author

Cameron MacKenzie

University of Notre Dame

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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Neuroscience· 2

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Anna WenningeriD· 2 shared Charles SanderiD· 2 shared Christopher PatzkeiD· 2 shared Jenny Bergqvist-PatzkeiD· 2 shared Alexander Weaver· 1 shared Alexandra NobleiD· 1 shared Alice A. BurchettiD· 1 shared Anis ContractoriD· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersNeuroscience

Anna WenningerORCID

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Author profile →

2 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