Author

C. Andrew Williams

University of Washington

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

Biology Disciplines

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Neuroscience· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:drug response / drug discovery· 1 Assay:proteomics· 1

Frequent Co-Authors

Jessica E. YoungiD· 2 shared Shannon E. Rose· 2 shared Allison KnuppiD· 1 shared Aquene N. ReidiD· 1 shared Chizuru Kinoshita· 1 shared Kyle J. TravagliniiD· 1 shared Panos TheofilasiD· 1 shared Refugio A. MartineziD· 1 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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2 shared papersNeuroscience

Jessica E. YoungORCID

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2 papers

Recent·Most cited

The Alzheimer's disease risk gene SORL1 is a regulator of excitatory neuronal function

C. Andrew Williams, Shannon E. Rose, Vera Stamenković, Aquene N. Reid, Kyle J. Travaglini, Stephen E.P. Smith, Jessica E. Young

This study shows that SORL1 deficiency in neurons alters synaptic protein interactions, causes hyperexcitability, and impairs synaptic plasticity, linking endosomal recycling defects to Alzheimer's disease pathogenesis.

Alzheimer s & Dementia · Sep 1, 2026Peer-reviewedNeuroscience

Pharmacologic Stabilization of Retromer Rescues Endosomal Pathology Induced by Defects in the Alzheimer's gene SORL1

Swati Mishra, Allison Knupp, Chizuru Kinoshita, C. Andrew Williams, Shannon E. Rose, Refugio A. Martinez, Panos Theofilas, Jessica E. Young

The paper tests if a retromer stabilizing drug, TPT-260, can correct endosomal and Alzheimer's-related pathologies in neurons with SORL1 variants.

bioRxiv · Jul 31, 2022 · PreprintNeuroscience