DYT1 is the most common monogenetic variant of generalized dystonia with a markedly reduced penetrance. So far, deep brain stimulation (DBS) is the only effective symptomatic treatment option of DYT1 dystonia, but the mechanisms involved are still enigmatic.
Dystonia is thought to result from maladaptive plasticity within central motor circuits, which may be triggered by environmental stressors such as peripheral trauma or overuse in individuals with an intrinsic (genetic) predisposition.
We will induce dystonia-like movements by forelimb overuse in transgenic rats harboring the human DYT1 mutation, and will characterize the evolution of motor symptoms, DBS effects, and pathophysiological changes on various neurobiological levels.
Team
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Prof. Jens Volkmann
Universitätsklinikum Würzburg
Deputy Spokesperson, Steering Committee Member, Project Leader
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Prof. Chi Wang Ip
Universitätsklinikum Würzburg
Project Leader
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Dr. Katarina Hofman
Universitätsklinikum Würzburg
Postdoc
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Priyansha Dubey
Universitätsklinikum Würzburg
PhD Student
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Dr. Lisa Rauschenberger
Universitätsklinikum Würzburg
Postdoc
Publications
Brain-to-gut trafficking of alpha-Synuclein by CD11c+ cells in a mouse model of Parkinson’s disease.
- Prof. Jens Volkmann
- Prof. Chi Wang Ip
Feasibility of local field potential-guided programming for deep brain stimulation in Parkinson’s disease: A comparison with clinical and neuro-imaging guided approaches in a randomized, controlled pilot trial.
- Prof. Cordula Matthies
- Prof. Jens Volkmann
Peripheral nerve injury elicits microstructural and neurochemical changes in the striatum and substantia nigra of a DYT-TOR1A mouse model with dystonia-like movements.
- Dr. Lisa Rauschenberger
- Dr. Susanne Knorr
- Prof. Jens Volkmann
- Prof. Chi Wang Ip
Expansion of regulatory T cells by CD28 superagonistic antibodies attenuates neurodegeneration in A53T-α-synuclein Parkinson’s disease mice.
- Dr. Susanne Knorr
- Prof. Chi Wang Ip
- Prof. Jens Volkmann
Age-dependent neurodegeneration and neuroinflammation in a genetic A30P/A53T double-mutated α-synuclein mouse model of Parkinson’s disease.
- Dr. Lisa Rauschenberger
- Dr. Alexander Grotemeyer
- Dr. Susanne Knorr
- Prof. Jens Volkmann
- Prof. Chi Wang Ip
Rodent models for gait network disorders in Parkinson’s disease – a translational perspective.
- Dr. Nikolaus Wenger
- Elisa Garulli
- Burçe Kabaoğlu
- Dr. Michael Schuhmann
- Prof. Chi Wang Ip
- Prof. Christoph Harms
- Prof. Matthias Endres
- Prof. Ioannis Isaias
- Prof. Philip Tovote
- PD Dr. Robert Blum
DRD1 signaling modulates TrkB turnover and BDNF sensitivity in direct pathway striatal medium spiny neurons.
- Dr. Thomas Andreska
- Daniel Wolf
- Maurilyn Ayon Olivas
- PD Dr. Robert Blum
- Prof. Jens Volkmann
- Prof. Chi Wang Ip
- Prof. Michael Sendtner
Deep brain stimulation electrode modeling in rats.
- Dr. Ningfei Li
- Konstantin Butenko
- Prof. Chi Wang Ip
- Prof. Andrea Kühn
- Dr. Andreas Horn
- Prof. Ursula van Rienen
Neurodegeneration by α-synuclein-specific T cells in AAV-A53T-α-synuclein Parkinson’s disease mice.
- PD Dr. Robert Blum
- Dr. Susanne Knorr
- Prof. Jens Volkmann
- Prof. Chi Wang Ip
Second hit hypothesis in dystonia: Dysfunctional cross talk between neuroplasticity and environment?
- Dr. Lisa Rauschenberger
- Dr. Susanne Knorr
- Prof. Jens Volkmann
- Prof. Chi Wang Ip