Author

Amy E. Easton

GenentechORCID 0000-0002-6864-4983Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:differential expression· 1 Approach:experimental assay· 1 Organism:human· 1 Organism:mouse· 1 Assay:proteomics· 1 Approach:statistical model· 1

Frequent Co-Authors

William J. MeilandtiD· 2 shared Alexander MunkiD· 1 shared Alvin GogineniiD· 1 shared Anne BieveriD· 1 shared Anubha MahajaniD· 1 shared Baris BingoliD· 1 shared Cong WuiD· 1 shared Hai NguiD· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersNeuroscience

William J. MeilandtORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

Intranigral injection of Alpha-Synuclein pre-formed fibrils leads to BBB compromise and Bilateral Dopaminergic Neurodegeneration in A53T Alpha-Synuclein transgenic mice.

Soumitra Ghosh, Han Lin, Sarah Chu, Hai Ngu, Nanzhi Zang, Renee Raman, Kimberly L. Stark, Oded Foreman, Somaye Sadat Hashemifar, Amy E. Easton, Baris Bingol, William J. Meilandt

This study develops a mouse model of Parkinson's disease by injecting alpha-synuclein pre-formed fibrils, leading to bilateral dopaminergic neurodegeneration and BBB compromise.

Discover Neuroscience · Aug 27, 2026Peer-reviewedNeuroscience

Therapeutically targeting the classical complement pathway with antisense oligonucleotides in Alzheimer's disease

Yuanyuan Wang, Tiffany Z. Wu, Alvin Gogineni, Ming‐Chi Tsai, Lukasz Jan Kielpinski, Anubha Mahajan, Shristi Pandey, Luis F. Schachner, John C. Tran, Cong Wu, Stephen P. Schauer, Anne Biever, Sidsel Boesen, Meiling Li, Alexander Munk, , Jesse E. Hanson

This study identifies the classical complement pathway as a therapeutic target in Alzheimer's disease and demonstrates the efficacy of antisense oligonucleotides in rescuing synapse loss in mouse models.

bioRxiv · Aug 23, 2024 · PreprintNeuroscience