Author

Milena Cioroch

University of Oxford

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Neuroscience· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Assay:imaging· 1 Organism:mouse· 1 Organism:rat· 1

Frequent Co-Authors

Natalie Connor‐RobsoniD· 2 shared Richard Wade‐MartinsiD· 2 shared Stephanie Jane CraggiD· 2 shared B Luther Davies· 1 shared Bradley M. RobertsiD· 1 shared Christopher MarshalliD· 1 shared Clare E. MackayiD· 1 shared David HautoniD· 1 shared

Activity by Year

2023-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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2 shared papersNeuroscience

Natalie Connor‐RobsonORCID

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2 papers

Recent·Most cited

A human GBA-L444P transgene drives early and persistent dopamine neurotransmission deficits and alpha-synuclein pathology in a mouse model of early Parkinson's disease

Natalie Connor‐Robson, Tara Diviney, Javier Alegre‐Abarrategui, Bradley M. Roberts, Katherine R. Brimblecombe, Nora Bengoa‐Vergniory, Harrison Waters, Milena Cioroch, B Luther Davies, Kateryna O. Bila, Martijn J. C. van der Lienden, Johannes M. F. G. Aerts, Stephanie Jane Cragg, Richard Wade‐Martins

This paper creates a humanised GBA-L444P mouse model to study GBA1 mutations in Parkinson's, finding gain-of-function effects on dopamine release and loss-of-function effects on alpha-synuclein pathology.

bioRxiv · May 27, 2026 · PreprintNeuroscience

Dopamine D2 receptor upregulation in dorsal striatum in the LRRK2-R1441C rat model of early Parkinson's disease revealed by in vivo PET imaging

Teresa Delgado‐Goñi, Natalie Connor‐Robson, Milena Cioroch, Stephen J. Paisey, Christopher Marshall, Emma L. Lane, David Hauton, James McCullagh, Peter J. Magill, Stephanie Jane Cragg, Clare E. Mackay, Richard Wade‐Martins, Johannes Christian Klein

The paper uses PET imaging to show increased dopamine D2 receptor binding in LRRK2-R1441C rats, suggesting receptor upregulation as a compensatory response to dopamine deficits.

bioRxiv · Aug 9, 2023 · PreprintNeuroscience