Author

Christiane Fahlbusch

Universitätsmedizin Göttingen

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 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

Ellen GerhardtiD· 3 shared Tiago F. OuteiroiD· 3 shared Ana MagalhãesiD· 1 shared C. Alexander BoeckeriD· 1 shared Dietmar RiedeliD· 1 shared Eftychia VasiliiD· 1 shared Erika CastilloiD· 1 shared Henning UrlaubiD· 1 shared

Activity by Year

2021-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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3 shared papersNeuroscience

Ellen GerhardtORCID

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Author profile →

3 papers

Recent·Most cited

LRRK2/LRRK1 interactions modulate Rab7 activity and inhibit lysosomal exocytosis

Madiha Mohieldin Merghani, Ellen Gerhardt, Maiken Hesse, Christiane Fahlbusch, C. Alexander Boecker, Tiago F. Outeiro

This study investigates the interaction between LRRK1 and LRRK2, showing they modulate Rab7 activity and lysosomal exocytosis, with starvation reducing their interaction and impairing lysosomal homeostasis.

bioRxiv · Jun 15, 2026 · PreprintCell Biology

Cofilin pathology is a new player on α-synuclein-induced spine impairment in models of hippocampal synucleinopathy

Marina I. Oliveira da Silva, Miguel Santejo, Isaac William Babcock, Ana Magalhães, Laurie S. Minamide, Seok-Joon Won, Erika Castillo, Ellen Gerhardt, Christiane Fahlbusch, Raymond A. Swanson, Tiago F. Outeiro, Ricardo Jorge Ferreira Taipa, Michael R. Ruff, James R. Bamburg, Márcia A. Liz

This study identifies cofilin dysregulation as a mediator of α-synuclein-induced synaptic dysfunction in hippocampal neurons in synucleinopathy models.

Cell Death and Disease · Apr 13, 2024Peer-reviewedNeuroscience

Common molecular mechanisms underlie the transfer of alpha-synuclein, Tau and huntingtin and modulate spontaneous activity in neuronal cells

Inês Caldeira Brás, Mohammad H. Khani, Eftychia Vasili, Wiebke Möbius, Dietmar Riedel, Iwan Parfentev, Ellen Gerhardt, Christiane Fahlbusch, Henning Urlaub, Markus Zweckstetter, Tim Gollisch, Tiago F. Outeiro

This study compares the release and effects of alpha-synuclein, Tau, and huntingtin in neuronal cells, showing similar release pathways and impacts on neuronal activity and inflammation.

bioRxiv · Jul 18, 2021 · PreprintNeuroscience