Author

John T. R. Isaac

National Institutes of HealthORCID 0000-0002-7946-1277Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:mouse· 3 Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Assay:electronic health records· 1 Assay:imaging· 1 Approach:statistical model· 1 Research Focus:trajectory inference· 1

Frequent Co-Authors

Aleksander P.F. DomanskiiD· 2 shared David J. A. WyllieiD· 2 shared Peter C. KindiD· 2 shared Sam A. BookeriD· 2 shared Adam D. JacksoniD· 1 shared Giles E. HardinghamiD· 1 shared James D. JohnsoniD· 1 shared Johanna JacksoniD· 1 shared

Activity by Year

2018-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersNeuroscience

Aleksander P.F. DomanskiORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

Differential aberrant structural synaptic plasticity in axons and dendrites ahead of their degeneration in tauopathy

Johanna Jackson, James D. Johnson, S. Meftah, Tracey K. Murray, Zeshan Ahmed, Matteo Fasiolo, Michael L. Hutton, John T. R. Isaac, Michael J. O’Neill, Michael C. Ashby

This study tracks synapse plasticity in tauopathy and finds that changes in synaptic structure precede neurite degeneration, with distinct patterns in axons and dendrites.

bioRxiv · Apr 29, 2020 · PreprintNeuroscience

Altered dendritic spine function and integration in a mouse model of Fragile X Syndrome

Sam A. Booker, Aleksander P.F. Domanski, Owen Dando, Adam D. Jackson, John T. R. Isaac, Giles E. Hardingham, David J. A. Wyllie, Peter C. Kind

This study shows that loss of FMRP in a mouse model of Fragile X Syndrome leads to increased single-spine excitation and more multiply-innervated spines, contributing to circuit hyperexcitability.

Nature Communications · Oct 23, 2019Peer-reviewedNeuroscience

Cellular and Synaptic Phenotype Compensations Limit Circuit Disruption in Fmr1-KO Mouse Layer 4 Barrel Cortex but Fail to Prevent Deficits in Information Processing

Aleksander P.F. Domanski, Sam A. Booker, David J. A. Wyllie, John T. R. Isaac, Peter C. Kind

The paper investigates how cellular and synaptic compensations in Fmr1-KO mice affect sensory processing in the barrel cortex, finding that despite compensatory mechanisms, sensory encoding precision is lost, leading to hypersensitivity.

bioRxiv · Nov 14, 2018 · PreprintNeuroscience