Author

Mihika Gangolli

Uniformed Services University of the Health SciencesORCID 0000-0002-8764-4313Unclaimed 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 Organism:human· 2 Research Focus:cell-cell communication· 1 Assay:imaging· 1 Organism:mouse· 1 Research Focus:spatial domain detection· 1

Frequent Co-Authors

David L. BrodyiD· 2 shared Andrew D. SauerbeckiD· 1 shared Christopher Hemingway· 1 shared David M. HoltzmaniD· 1 shared Martin KerschensteineriD· 1 shared Maud GratuzeiD· 1 shared Maverick H. Salyards· 1 shared Nigel J. CairnsiD· 1 shared

Activity by Year

2018-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersNeuroscience

David L. BrodyORCID

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2 papers

Recent·Most cited

SEQUIN multiscale imaging of mammalian central synapses reveals loss of synaptic microconnectivity resulting from diffuse traumatic brain injury

Andrew D. Sauerbeck, Mihika Gangolli, Sydney J. Reitz, Maverick H. Salyards, Samuel Kim, Christopher Hemingway, Maud Gratuze, Tejaswi Makkapati, Martin Kerschensteiner, David M. Holtzman, David L. Brody, Terrance T. Kummer

This paper introduces SEQUIN, a super-resolution imaging workflow for analyzing synapses, and shows synapse loss in traumatic brain injury and Alzheimer's models.

Neuron · May 8, 2020Peer-reviewedNeuroscience

Soluble amyloid-beta buffering by plaques in Alzheimer disease dementia versus high-pathology controls

Thomas J. Esparza, Mihika Gangolli, Nigel J. Cairns, David L. Brody

The paper investigates whether amyloid-beta plaques sequester toxic soluble Aβ aggregates in Alzheimer disease dementia, finding no significant difference in Aβ binding between dementia and high-pathology control groups.

PLoS ONE · Jul 6, 2018Peer-reviewedNeuroscience