Author

David Isaac Finkelstein

The University of MelbourneORCID 0000-0002-8167-4917Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:differential expression· 3 Approach:experimental assay· 3 Research Focus:cell type annotation· 2 Research Focus:cell-cell communication· 2 Organism:human· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Organism:Drosophila· 1

Frequent Co-Authors

An ChengiD· 1 shared Andrew Francis HilliD· 1 shared Asheeta A. PrasadiD· 1 shared Baiyao Liu· 1 shared Carolyn M. SueiD· 1 shared Cathryn L. UgaldeiD· 1 shared Chuantao Wu· 1 shared Clare L. ParishiD· 1 shared

Activity by Year

2019-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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1 shared paperNeuroscience

An ChengORCID

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Author profile →

4 papers

Recent·Most cited

Transgenic A53T mice have astrocytic α-synuclein aggregates in dopamine and striatal regions

Cormac Peat, Asheeta A. Prasad, David Isaac Finkelstein, Carolyn M. Sue, Jennifer A. Johnston, Clare L. Parish, Lachlan H. Thompson, Deniz Kirik, Glenda Margaret Halliday

This study shows that astrocytes in the substantia nigra pars compacta of A53T transgenic mice have more -synuclein aggregates and reactive morphology compared to wild-type mice.

Neuropathology and Applied Neurobiology · Aug 1, 2026Peer-reviewedNeuroscience

Astrocytic FABP5 drives non-cell-autonomous oligodendrocyte injury in multiple system atrophy by promoting TNF signaling and ferroptotic stress

Chuantao Wu, Jiejing Lin, Yi Chen, Nozomi Takahashi, Qikai Chen, Baiyao Liu, Fan Dai, Wenxue Zhao, David Isaac Finkelstein, K. Kawahata, Kohji Fukunaga, An Cheng

This study identifies FABP5 as a key driver of astrocyte-mediated oligodendrocyte injury in MSA by promoting TNF signaling and ferroptotic stress.

Redox Biology · Apr 3, 2026Peer-reviewedNeuroscience

SNCAE46K transgenic Drosophila Model of Parkinsons Disease Confirmed the Causative Role of Oxidative Stress

Samaneh Reiszadeh Jahromi, S. R. Ramesh, David Isaac Finkelstein, Mohammad Haddadi

This study creates a Drosophila model overexpressing the E46K mutant SNCA gene, confirming its role in inducing oxidative stress and neurodegeneration associated with Parkinson's disease.

bioRxiv · Feb 28, 2020 · PreprintNeuroscience

Misfolded α-synuclein causes hyperactive respiration without functional deficit in live neuroblastoma cells

Cathryn L. Ugalde, Sarah Jane Annesley, Shane E. Gordon, Katelyn H. Mroczek, Matthew A. Perugini, Victoria Lawson, Paul R. Fisher, David Isaac Finkelstein, Andrew Francis Hill

The paper shows misfolded α-synuclein, generated via PMCA, binds cardiolipin and causes hyperactive mitochondrial respiration in neuroblastoma cells without functional deficits.

Disease Models & Mechanisms · Dec 17, 2019Peer-reviewedNeuroscience