Author

Ayman H. Faroqi

Mayo ClinicORCID 0000-0002-1659-753XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Research Focus:differential expression· 2 Organism:human· 2 Organism:mouse· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1

Frequent Co-Authors

Jeremy D. BurgessiD· 2 shared Marion DelenclosiD· 2 shared Natasha N. DeMeoiD· 2 shared Pamela J. McLeaniD· 2 shared Danilyn Amerna· 1 shared Drew J. Quiriconi· 1 shared Fabienne C. FieseliD· 1 shared Iva StojkovskaiD· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersNeuroscience

Jeremy D. BurgessORCID

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2 papers

Recent·Most cited

NeuroscienceFrontiers in Aging NeurosciencePeer-reviewedAug 10, 2023

Honokiol decreases alpha-synuclein mRNA levels and reveals novel targets for modulating alpha-synuclein expression.

Sara J. Fagen, Jeremy D. Burgess, Melina J. Lim…·Pamela J. McLean

This study shows honokiol reduces alpha-synuclein mRNA and protein levels in models of Parkinson's disease by modulating SNCA gene expression, identifying potential therapeutic targets.

5 citations

humanmouse

𝕏 PostBluesky

NeuroscienceMolecular NeurodegenerationPeer-reviewedJan 13, 2020

Alpha-synuclein-induced mitochondrial dysfunction is mediated via a sirtuin 3-dependent pathway.

Jae Hyeon Park, Jeremy D. Burgess, Ayman H. Faroqi…·Pamela J. McLean

This study shows that alpha-synuclein oligomers reduce mitochondrial SIRT3 activity, impair mitochondrial dynamics, and that AICAR treatment restores SIRT3 and improves mitochondrial dysfunction in Parkinson's disease models.

189 citationstop 1%

mousehuman

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