Author

Clayton A. Farris

Washington University in St. Louis

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Neuroscience· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Assay:electronic health records· 2 Organism:mouse· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Approach:experimental assay· 1 Approach:statistical model· 1

Frequent Co-Authors

Eva L. DyeriD· 2 shared Halla ElmoreiD· 2 shared James N. McGregoriD· 2 shared Keith B. HengeniD· 2 shared Kiran Bhaskaran‐Nair· 2 shared Aidan M SchneideriD· 1 shared Chao WangiD· 1 shared David M. HoltzmaniD· 1 shared

Activity by Year

2022-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 41 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

Eva L. DyerORCID

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Tauopathy severely disrupts homeostatic set-points in emergent neural dynamics but not in the activity of individual neurons.

James N. McGregor, Clayton A. Farris, Sahara Ensley, Aidan M Schneider, Chao Wang, Yuqi Liu, Jianhong Tu, Halla Elmore, Keenan D. Ronayne, Ralf Weßel, Eva L. Dyer, Kiran Bhaskaran‐Nair, David M. Holtzman, Keith B. Hengen

This study shows that tauopathy disrupts network-level homeostatic set-points in hippocampal activity but not individual neuron activity, with implications for computational capacity and behavior.

bioRxiv · Sep 1, 2023 · PreprintNeuroscience

Circuit-specific selective vulnerability in the DMN persists in the face of widespread amyloid burden.

Samuel J. Brunwasser, James N. McGregor, Kiran Bhaskaran‐Nair, Clayton A. Farris, Halla Elmore, Eva L. Dyer, John M. Grady, Jennifer D. Whitesell, Julie A. Harris, Keith B. Hengen

The paper investigates circuit-specific vulnerability in the default mode network (DMN) in Alzheimer's disease, finding that dysfunction is restricted to in-DMN projecting circuits despite widespread amyloid burden.

bioRxiv · Nov 14, 2022 · PreprintNeuroscience