Author

Toru Yamamoto

Niigata UniversityORCID 0000-0002-2464-4236Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

Click to filter author papers

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:mouse· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Assay:electronic health records· 1

Frequent Co-Authors

Soju SekiiD· 2 shared Antonios PantazisiD· 1 shared Emiko Tanaka IsomuraiD· 1 shared Igor SpigelmaniD· 1 shared Kazuaki MiyagawaiD· 1 shared Kiara N. QuinniD· 1 shared Martina Wiedau‐PazosiD· 1 shared Masayuki OnoiD· 1 shared

Activity by Year

2019-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 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 papersNeuroscience

Soju SekiORCID

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Sensory neuron dysfunction and hyperexcitability in dorsal root ganglia at disease onset in the SOD1G93A mouse model of ALS.

輝西浦, Soju Seki, Takuhiro Kobayashi, Yoshihiro Kitaoka, Sou Kawata, Toru Yamamoto, Kazuaki Miyagawa, Toshihiro Uchihashi, Yosuke Ohtake, Takahide Itokazu, Toshihide Yamashita, Masayuki Ono, Yusuke Yokota, Emiko Tanaka Isomura, Susumu Tanaka

The paper identifies early molecular, structural, and functional changes in sensory neurons in the SOD1G93A mouse model of ALS, suggesting sensory neuron hyperexcitability as a potential therapeutic target.

bioRxiv · Sep 1, 2026 · PreprintNeuroscience

Circuit-Specific Early Impairment of Proprioceptive Sensory Neurons in the SOD1G93A Mouse Model for ALS

Soju Seki, Toru Yamamoto, Kiara N. Quinn, Igor Spigelman, Antonios Pantazis, Riccardo Olcese, Martina Wiedau‐Pazos, Scott H. Chandler, Sharmila Venugopal

The paper identifies early proprioceptive sensory neuron impairments in SOD1G93A mice, showing Nav1.6 channel deficits and reflexive defects in ALS.

Journal of Neuroscience · Sep 17, 2019Peer-reviewedNeuroscience