Author

Francesco Paonessa

University of CambridgeORCID 0000-0002-4729-0928Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:Drosophila· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Assay:imaging· 1 Assay:spatial transcriptomics· 1

Frequent Co-Authors

Frederick J. LiveseyiD· 3 shared Delphine LarrieuiD· 2 shared Alexander J. WhitworthiD· 1 shared Andrea H. BrandiD· 1 shared Bernardo Delarue Bizzini· 1 shared Caroline C. G. FabreiD· 1 shared Catherine M. Davidson· 1 shared Deepthy Francis· 1 shared

Activity by Year

2018-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersNeuroscience

Frederick J. LiveseyORCID

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3 papers

Recent·Most cited

Cell BiologyOpen BiologyPeer-reviewedMay 13, 2026

Essential conserved neuronal motors kinesin-1 and kinesin-3 regulate Abeta42 toxicity in vivo

Deepthy Francis, Francesco Paonessa, Victoria L. Hewitt…·Isabel M. Palacios

This study shows that kinesin-1 and kinesin-3 mitigate Aβ42Arc toxicity in Drosophila neurons and rescue behavioral defects.

1 citation

Drosophilaspatial transcriptomics

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NeurosciencebioRxivPreprintOct 19, 2024

Targeting the acetyltransferase NAT10 corrects pathologies in human frontotemporal dementia neurons and extends lifespan in an in vivo Drosophila tauopathy model

Francesco Paonessa, Bernardo Delarue Bizzini, Tom Campbell…·Frederick J. Livesey

The paper shows that inhibiting NAT10 corrects nuclear defects and extends lifespan in tauopathy models.

1 citation

humanDrosophila

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NeurosciencebioRxivPreprintMay 22, 2018

Abnormal microtubule dynamics disrupt nucleocytoplasmic transport in tau-mediated frontotemporal dementia

Francesco Paonessa, Lewis Evans, Rekha Solanki…·Frederick J. Livesey

This study shows that tau mutations in FTD cause hyperphosphorylation, mislocalization, and nuclear membrane deformation, leading to defective nucleocytoplasmic transport.

1 citation

humanexperimental assay

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