Author

Anna S. Blazier

Sanofi (France)Primary ORCID profile (0000-0001-5226-0339 · 1 paper)Unclaimed ORCID profile · follow to get notified of new preprints

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Same name, identified by ORCID

Anna S. BlazieriD1 paper · University of Virginia

Biology Disciplines

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Immunology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Assay:scRNA-seq· 2 Approach:statistical model· 2 Research Focus:cell-cell communication· 1 Approach:deep learning· 1 Organism:human· 1 Organism:mouse· 1

Frequent Co-Authors

Dimitry OfengeimiD· 2 shared Bailin ZhangiD· 1 shared Daniel S. ReichiD· 1 shared Devan Moodley· 1 shared Disha SoodiD· 1 shared Ellen D. Cahir-McFarlandiD· 1 shared Eric B. DammeriD· 1 shared Erin BeckiD· 1 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersImmunology

Dimitry OfengeimORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

Maintenance of chronic neuroinflammation in multiple sclerosis via interferon signaling and CD8 T cell-mediated cytotoxicity

Syed Ali Raza, Yoshimi Enose‐Akahata, Anna S. Blazier, Lauren Guerra, Erin Beck, María Inés Gaitán, Nyater Ngouth, Jefte M. Drijvers, Eric B. Dammer, Devan Moodley, Kory R. Johnson, Martina Absinta, Valeria Ramaglia, Jennifer L. Gommerman, Timothy Turner, , Daniel S. Reich

This study identifies chronic neuroinflammation in MS through scRNA-seq and proteomics, showing persistent IFN signaling and CD8 T cell cytotoxicity despite B-cell depletion.

bioRxiv · Jun 9, 2025 · PreprintImmunology

Glial state changes and neuroinflammatory RIPK1 signaling are a key feature of ALS pathogenesis

Matija Zelic, Anna S. Blazier, Fabrizio Pontarelli, Michael J. LaMorte, Jeremy Y. Huang, Ozge E. Tasdemir-Yilmaz, Yi Ren, Sean K. Ryan, Pavithra Krishnaswami, Mikhail N. Levit, Disha Sood, Yao Chen, Joseph Gans, Xinyan Tang, Jennifer Hsiao‐Nakamoto, , Timothy R. Hammond

This study identifies glial state changes and RIPK1 signaling as key features of ALS pathogenesis, showing that blocking RIPK1 delays disease onset and modulates glial responses.

bioRxiv · Apr 12, 2024 · PreprintNeuroscience