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Funded Studies

Thomas Gasser, MD, PhD

Director, Department of Neurodegeneration at Hertie Institute for Clinical Brain Research

Location: Tuebingen Germany

Dr.Gasser is a professor of neurology and has been director of the Department of Neurodegenerative Diseases at the Hertie-Institute for Clinical Brain Research since 2002 and chairman of the Board of Directors at the Center of Neurology, University of Tuebingen, Germany since 2007. In 2010 he became dean of research of the Medical Faculty at the University of Tuebingen and since 2013 he has also been coordinator for clinical studies at the Tuebingen partner of the German Center for Neurodegenerative Diseases (DZNE).

Professor Gasser studied medicine at the University of Freiburg, Germany, and at Yale University Medical School. He received his professional training in psychiatry at the Max Planck-Institute of Psychiatry and in neurology at the Department of Neurology of the University of Munich. From 1991 to 1993 he trained as a post-doctoral fellow with a stipend of the German Research Foundation at Harvard Medical School in the laboratory of Professor Xandra Breakefield. He returned to Munich to become assistant professor in neurology and head of the Neurogenetics Unit as well as the Movement Disorders Outpatient Unit before moving to his present position.

His main areas of research are the genetic and molecular basis of Parkinson’s disease, dystonias and other movement disorders, including the mapping, cloning and functional characterization of Mendelian genes causing Parkinson’s disease and other movement disorders, as well as their diagnosis and treatment but also the identification of common genetic variability which contributes to the sporadic forms of the disease.

Associated Grants

  • Evaluation of LRRK2 Kinase Activity in Blood Cells


  • Deciphering the Genetic Architecture of the LRRK2 Gene in the Indian Population


  • Assessing the Role of LRRK2 in Sporadic Parkinson’s Disease Using iPSC-derived Dopaminergic Neurons


  • Functional Analysis of LRRK2 Phosphorylation in Human Dopaminergic Neurodegeneration


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