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Dorothee Dormann

Dorothee Dormann


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Dorothee Dormann is professor of molecular cell biology in the Faculty of Biology at Johannes Gutenberg University (JGU) Mainz and adjunct director at the Institute of Molecular Biology (IMB) Mainz. She is co-leading the Elucidating the Mechanisms of FUS-Linked ALS project.

Dormann studied biochemistry in Tübingen (Germany) and obtained a PhD in cell biology/immunology from Rockefeller University, New York (US). In 2007 she joined the laboratory of Christian Haass at LMU Munich as a postdoctoral fellow, investigating the cellular and molecular mechanisms that underlie neurodegenerative diseases, in particular amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). In 2014 she became an independent research group leader at the BioMedical Center of LMU Munich. In 2021 she was awarded a Heisenberg Professorship and a Gutenberg Research College Fellowship to join JGU Mainz as full professor.

Dormann’s research focuses on nucleocytoplasmic transport, phase separation and post-translational modifications of neurodegeneration-linked RNA-binding proteins and how these mechanisms are disturbed in disease, in particular ALS, FTD and Alzheimer’s disease. Her goal is to decipher the molecular mechanisms that underlie RNA-binding protein mislocalization and aggregation in the context of neurodegenerative diseases. She also aims to understand the physiological functions of neurodegeneration-linked RNA-binding proteins, how they are regulated and how dysfunctional RNA-binding proteins cause neurodegeneration. Dormann’s long-term goal is to understand the control mechanisms that maintain cellular stress resilience and protect against protein aggregation and neurodegeneration, thereby allowing healthy aging.

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Abstract: Cytoplasmic aggregation and concomitant nuclear clearance of the RNA-binding protein TDP-43 are found in ~ 90% of cases of amyotrophic lateral sclerosis and ~ 45% of patients living with frontotemporal lobar degeneration, but no disease-modifying therapy is available. Antibody therapy targeting other aggregating proteins associated with neurodegenerative disorders has shown