Author

Jonathan C. Neumann

University of California, Irvine

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

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Neuroscience· 6

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Organism:mouse· 6 Research Focus:cell type annotation· 5 Research Focus:differential expression· 5 Approach:experimental assay· 4 Assay:bulk RNA-seq· 2 Research Focus:cell-cell communication· 2 Assay:spatial transcriptomics· 2 Approach:statistical model· 2

Frequent Co-Authors

Grant R. MacGregoriD· 6 shared Kim N. GreeniD· 5 shared Shimako KawauchiiD· 5 shared Andrea J. TenneriD· 4 shared Celia Da Cunha· 4 shared Frank M. LaFerlaiD· 4 shared Kristine M. TraniD· 4 shared Ali MortazaviiD· 3 shared

Activity by Year

2019-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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6 shared papersNeuroscience

Grant R. MacGregorORCID

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6 papers

Recent·Most cited

Generation of an inducible destabilized-domain Cre mouse line to target disease associated microglia

Caden M. Henningfield, M. Ngo, Kaitlin M. Murray, Nellie E. Kwang, Kate Inman Tsourmas, Jonathan C. Neumann, Zachary A. Pashkutz, Shimako Kawauchi, Vivek Swarup, Thomas E. Lane, Grant R. MacGregor, Kim N. Green

The paper develops a mouse model to specifically target disease-associated microglia (DAMs) using an inducible Cre system and validates its specificity through spatial transcriptomic analysis.

Glia · Feb 23, 2025Peer-reviewedNeuroscience

APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology

Kristine M. Tran, Nellie E. Kwang, Claire Ann Butler, Ángela Gómez-Arboledas, Shimako Kawauchi, Cassandra Mar, Donna Chao, Rocio A. Barahona, Celia Da Cunha, Kate Inman Tsourmas, Zechuan Shi, Shuling Wang, Sherilyn Collins, Amber Walker, Kai‐Xuan Shi, , Kim N. Green

The paper investigates how the APOE Christchurch variant affects microglial responses to amyloid and tau pathology in mouse models, finding it enhances plaque-related responses but suppresses tau-related inflammation.

Molecular Neurodegeneration · Jan 22, 2025Peer-reviewedNeuroscience

A Trem2*R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques

Kristine M. Tran, Shimako Kawauchi, Enikö A. Kramár, Narges Rezaie, Heidi Yahan Liang, Jasmine Sakr, Ángela Gómez-Arboledas, Miguel A. Arreola, Celia da Cunha, Jimmy Phan, Shuling Wang, Sherilyn Collins, Amber Walker, Kai‐Xuan Shi, Jonathan C. Neumann, , Kim N. Green

Molecular Neurodegeneration · Feb 17, 2023Peer-reviewedNeuroscience

Systematic phenotyping and characterization of the 3xTg-AD mouse model of Alzheimer's Disease

Dominic I. Javonillo, Kristine M. Tran, Jimmy Phan, Edna E. Hingco, Enikö A. Kramár, Celia da Cunha, Stefânia Forner, Shimako Kawauchi, Giedre Milinkeviciute, Ángela Gómez-Arboledas, Jonathan C. Neumann, Crystal E. Banh, Michelle Dieu Thao Huynh, Dina P. Matheos, Narges Rezaie, , Frank M. LaFerla

This paper characterizes the 3xTg-AD mouse model of Alzheimer's Disease across its lifespan and compares it with the 5xFAD model to assess pathology and model drift.

Frontiers in Neuroscience · Jan 24, 2022Peer-reviewedNeuroscience

Systematic Phenotyping and Characterization of the 5xFAD mouse model of Alzheimer's Disease

Stefânia Forner, Shimako Kawauchi, Gabriela Balderrama-Gutierrez, Enikö A. Kramár, Dina P. Matheos, Jimmy Phan, Dominic I. Javonillo, Kristine M. Tran, Edna E. Hingco, Celia da Cunha, Narges Rezaie, Joshua A. Alcantara, David Baglietto‐Vargas, Camden S. Jansen, Jonathan C. Neumann, , Kim N. Green

The paper performs a comprehensive phenotypic analysis of the 5xFAD mouse model across its lifespan, identifying novel age-related pathological features.

Scientific Data · Oct 15, 2021Peer-reviewedNeuroscience

Interneuron dysfunction in a new knock-in mouse model of SCN1A GEFS+

Antara Das, Bingyao Zhu, Yunyao Xie, Lisha Zeng, An T. Pham, Jonathan C. Neumann, Grant R. MacGregor, Soleil Sun Schutte, Robert F. Hunt, Diane K. O’Dowd

This study introduces a mouse model with a SCN1A mutation linked to GEFS+ and shows that heterozygous mutants develop seizures due to impaired inhibitory interneuron function.

bioRxiv · Nov 21, 2019 · PreprintNeuroscience