Author

Wenyan Sun

Tulane UniversityORCID 0000-0002-3186-5002Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

Click to filter author papers

Neuroscience· 2 Genomics· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:differential expression· 3 Assay:bulk RNA-seq· 2 Approach:experimental assay· 2 Organism:mouse· 2 Assay:DNA methylation· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1 Approach:statistical model· 1

Frequent Co-Authors

Bess E FrostiD· 2 shared Paulino RamireziD· 2 shared Adrian BeckmanniD· 1 shared Angela BarattiniiD· 1 shared Bernard FongangiD· 1 shared Bradley T. HymaniD· 1 shared Elizabeth OchoaiD· 1 shared Ethan R. RoyiD· 1 shared

Activity by Year

2021-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersGenomics

Bess E FrostORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Ischemia-reperfusion and acidosis induce retrotransposon derepression in the mouse brain

Youfang Zhou, Angela Barattini, Xiang‐ming Zha, Wenyan Sun

This study shows ischemia-reperfusion and acidosis increase retrotransposon expression in mouse brain tissue, suggesting a role in ischemic injury.

bioRxiv · Aug 7, 2026 · PreprintNeuroscience

Nanopore Long-Read Sequencing Unveils Genomic Disruptions in Alzheimer's Disease

Paulino Ramirez, Wenyan Sun, Shiva Kazempour Dehkordi, Habil Zare, Giovanni Pascarella, Piero Carninci, Bernard Fongang, Kevin F. Bieniek, Bess E Frost

This study uses nanopore long-read sequencing to analyze genomic disruptions in Alzheimer's disease, finding increased retrotransposon activity and structural variants in aged brains.

Alzheimer s & Dementia · Nov 1, 2025Peer-reviewedGenomics

Pathogenic tau accelerates aging-associated activation of transposable elements in the mouse central nervous system

Paulino Ramirez, Gabrielle Zuniga, Wenyan Sun, Adrian Beckmann, Elizabeth Ochoa, Sarah L. DeVos, Bradley T. Hyman, Gabriel S. Chiu, Ethan R. Roy, Wei Cao, Miranda E. Orr, Virginie Buggia-Prévot, William J. Ray, Bess E Frost

This study shows that pathogenic tau accelerates transposable element activation in the aging mouse brain, particularly ERVs, suggesting a link between tauopathy and transposable element-induced neurotoxicity.

Progress in Neurobiology · Oct 18, 2021Peer-reviewedNeuroscience