Author

Ching‐On Wong

Rutgers, The State University of New JerseyORCID 0000-0002-8602-2125Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 2

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Bidisha RoyiD· 1 shared Elham RastegariiD· 1 shared Ho Hang LeungiD· 1 shared Hugo Jozef BelleniD· 1 shared Kai Li TaniD· 1 shared Kartik VenkatachalamiD· 1 shared Maciej JeziorekiD· 1 shared Nicholas E. KaragasiD· 1 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperNeuroscience

Bidisha RoyORCID

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2 papers

Recent·Most cited

TMEM55B downregulation promotes neurodegeneration in Alzheimer disease models.

Bidisha Roy, Viorica Raluca Contu, Maciej Jeziorek, Wilma Friedman, Ching‐On Wong

The paper shows TMEM55B downregulation contributes to neurodegeneration in Alzheimer's disease models by impairing lysosomal transport and autophagy.

bioRxiv · Oct 24, 2026 · PreprintNeuroscience

Loss of Activity-Induced Mitochondrial ATP Production Underlies the Synaptic Defects in a Drosophila model of ALS

Nicholas E. Karagas, Richa Gupta, Elham Rastegari, Kai Li Tan, Ho Hang Leung, Hugo Jozef Bellen, Kartik Venkatachalam, Ching‐On Wong

This paper identifies bioenergetic dysfunction due to reduced activity-induced mitochondrial ATP production as the cause of synaptic defects in a Drosophila ALS model.

Journal of Neuroscience · Sep 8, 2022Peer-reviewedNeuroscience