Ip Lab

People

Top, left to right:Thomas Musacchio, Lukas Schweizer, Heike Menzel, Susanne Knorr. Middle: Yaser Al-Zuraiqi, Mohammad Badr, Yin Jing, Louisa Frieß, Chi Wang Ip. Bottom: Lisa Rauschenberger, Akua Karikari, Alea Stengl, Keali Röhm

Contact

PD Dr. Chi Wang Ip

Group leader, Department of Neurology

ip_c@ukw.de

Josef-Schneider-Strasse 11, 97080 Würzburg

Publications (selected list)

Musacchio T, Rebenstorff M, Fluri F, Brotchie JM, Volkmann J, Koprich JB, Ip CW. STN-DBS is neuroprotective in the A53T α-synuclein Parkinson's disease rat model. Ann Neurol. 2017 May 3. doi: 10.1002/ana.24947

 

Ip CW, Cheong D, Volkmann J. Stereological Estimation of Dopaminergic Neuron Number in the Mouse Substantia Nigra Using an Optical Fractionator and Standard Microscopy Equipment. J. Vis. Exp., e56103, doi:10.3791/56103 (2017), in-press

 

Ip CW, Klaus LC, Karikari AA, Visanji NP, Brotchie JM, Lang AE, Volkmann J, Koprich JB. AAV1/2-induced overexpression of A53T-α-synuclein in the substantia nigra results in degeneration of the nigrostriatal system with Lewy-like pathology and motor impairment: a new mouse model for Parkinson's disease. Acta Neuropathol Commun. 2017, Feb 1;5(1):11. doi: 10.1186/s40478-017-0416-x.

 

Ip CW, Isaias IU, Kusche-Tekin BB, Klein D, Groh J, O'Leary A, Knorr S, Higuchi T, Koprich JB, Brotchie JM, Toyka KV, Reif A, Volkmann J. Tor1a+/- mice develop dystonia-like movements via a striatal dopaminergic dysregulation triggered by peripheral nerve injury. Acta Neuropathol Commun. 2016 Oct 3;4(1):108.

 

Ip CW, Beck SK, Volkmann J. Lymphocytes reduce nigrostriatal deficits in the 6-hydroxydopamine mouse model of Parkinson's disease. J Neural Transm. 2015, Aug 20.

Research

Video on JoVE: Stereological Estimation of Dopaminergic Neuron Number in the Mouse Substantia Nigra Using the Optical Fractionator and Standard Microscopy Equipment

Project 1:

To assess the impact of the immune system on Parkinson’s disease (PD) progression, we generated a novel mouse model for PD by injection of a viral vector into the Substantia nigra (SN) leading to overexpression of the A53T variant of alpha-synuclein (aSyn). Aim of this project is to analyze the relevant components of the immune system and aSyn antigenicity in this mouse model by immunohistochemistry, FACS analysis for different immune cell subtypes and activation status and cytokine bead arrays. This is conducted in cooperation with Professor Manfred Lutz, Institute of Virology and Immunobiology, Würzburg. We will carry out A53T aSyn injections into transgenic mice and perform additional adoptive transfer experiments with different lymphocytic subpopulation. Subsequent behavioral, histological and immunological investigations will then give unravel the role of the immune system in this mouse model of PD.

In a clinical part of this project, we will analyze blood samples of Parkinson’s disease patients for humoral and cellular components of the immune system with focus on aSyn.

 

Project 2:

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an established method for treatment of Parkinson’s disease patients. This project deals with neurobiological changes of STN-DBS in a Parkinson’s disease rat model. Data suggest a neuroprotective effect of STN-DBS, therefore we aim to analyse the mechanism leading to neuroprotection by using immunohistochemistry, mRNA and Western blot analyses. For this project we collaborate with Professor James Koprich and Professor Jonathan Brotchie from the Toronto Western Research Institute, Canada.

 

Project 3:

Aim of this project is to investigate central network changes in posttraumatic and overuse dystonia in mouse and rat models for monogenetic dystonia like DYT1 and DYT12. We implement morphological techniques like Golgi-Cox stainings to analyze dendritic arborization within the striatum, stereological analyses of striatal interneurons, functional investigations of neurotransmitter binding by autoradiography and neurobiological techniques like mRNA, Western blot analyses and microdialysis/HPLC to assess the mechanisms underlying central network abnormalities in rodent models for dystonia. Moreover, network changes in the basal ganglia-cerebellar-thalamic-cortex loop will be examined in dystonia as well as central network changes after deep brain stimulation. In this project we cooperate with PD Dr. Kathrin Grundmann-Hauser from the Institute of Medical Genetics and Applied Genomics, Tübingen.

© 2019 by Philip Tovote

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last update: 20/11/2019