contact & imprint
Virus

Fellows:

Laura Emily Clemens

 
Education and work experience

03/2015 – present

Experienced researcher at QPS Austria, Austria
Research and Development, Animal Facility Unit

04/2009 – 02/2015

Researcher and Ph.D. candidate at the University of Tuebingen, Germany
Institute of Medical Genetics and Applied Genomics, Huntington Disease Group

10/2004 – 03/2009

Research assistant and Diploma student at the University of Marburg, Germany.
Department of Animal Physiology

10/2001 – 09/2004

Diploma student at the University of Frankfurt, Germany.
Department of Biology

Work to be performed within SwitchHD:

1.

Metabolic dysfunction in BACHD rats
BACHD rats show metabolic abnormalities already at the early age of 1 month. Most prominently, the rats display a reduced body size and obesity (Jansson & Clemens et al., 2014). Pilot studies suggest that this is the result of reduced growth hormone availability and impaired lipid utilization (Clemens & Yu-Taeger et al., unpublished). There are further indications that the altered body constitution of BACHD rats might confound outcomes of behavioral studies working with food reward, unless the food deprivation regime is adapted (Jansson & Clemens et al., 2014). The aim is to validate these results by investigating feeding behavior and performing serum and histological brain analyses.

2.

Cognitive dysfunction in BACHD rats
BACHD rats show reversal learning deficits in several cognitive tasks (Abada et al., 2013; Clemens & Weber et al., in revision; Jansson et al., unpublished). It is of interest to evaluate, if the deficits originate from striatal or hippocampal disturbances by the use several maze setups that differentially affect these two brain regions.

3.

Inactivation of mutant huntingtin in different primary BACHD rat neurons
The major aim of SwitchHD is the inactivation of mutant huntingtin in different areas of the brain to investigate their contribution to the disease pathogenesis. Primary striatal, cortical and hypothalamic neurons are screened for mutant huntingtin-related disruption of molecular pathways of cell energy metabolism, survival and death by means of gene silencing.

Benedikt Fabry

 
Education and Work Experience

02/2016 - present

Experienced researcher at QPS Austria, Austria Research and Development, Animal Facility Unit

03/2012 - 01/2016

Researcher and Ph.D. candidate at the University of Tuebingen, Germany
Institute of Medical Genetics and Applied Genomics

10/2011 - 02/2012

Research assistant at the University of Tuebingen, Center for Plant Molecular Biology

10/2006 - 09/2011

Diploma student ath the University of Hohenheim, Germany
Department of Biology

SWITCH-HD
Inactivation of mutant huntingtin in different primary BACHD rat neurons.

The major aim of SwitchHD is the inactivation of mutant huntingtin in different areas of the brain to investigate their contribution to the disease pathogenesis. Primary striatal, cortical and hypothalamic neurons are screened for mutant huntingtin-related disruption of molecular pathways of cell energy metabolism, survival and death by means of gene silencing.

Arianna Novati

 

Arianna Novati is a biologist with background in in the fields of animal physiology and behavioral neuroscience. Currently she is a postdoctoral fellow in the Switch HD project, transferred from QPS Austria to the University of Tuebingen (EKUT). Her work within the project aims to contribute to the behavioral characterization of the BACHD rat model and will focus on depressive like behavior, maternal care and sexual behavior. Her research will include also analyses of molecular markers related to behavioral phenotypes as well as brain epigenetic changes associated to environmental manipulations in BACHD rats. Her secondment is meant to convey experience on test procedures for cognitive deficits in rats from QPS to EKUT and transfer knowledge on psychiatric like symptoms in BACHD rats back to QPS.

Janice Stricker-Shaver

 
Education

2003 – 2006

Bachelor of Science (Food and Nutritional Science)
University of Hong Kong, Hong Kong

2006 – 2010

Doctor of Philosophy (Molecular Biology)
University of Hong Kong, Hong Kong

Working experience

2011 – 2012

Postdoctoral Fellow (Regenerative medicine)
National Institute for Materials Science (NIMS), Japan

2012 – 2014

Postdoctoral Research Associate (Neurodegeneration and gene therapy)
University of Sheffield, United Kingdom

2014 – 2015

Postdoctoral Fellow (Neuroimaging)
Max Planck Institute for Biological Cybernetics, Germany

2015.02 – Present

Postdoctoral Fellow (Neurodegeneration)
University of Tuebingen, Germany

SWITCH-HD
Huntington disease is an autosomal dominantly inherited neurodegenerative disorder with no effective treatment at present. In this project, the effects of down-regulating the mutant huntingtin on rescuing the HD symptoms in the transgenic BACHD model will be investigated using a gene therapy approach coupled to neuroimaging, neuropathological and behavioural analyses. I will be delivering a viral-based vector for inactivating mutant huntingtin in the hypothalamus and characterize the treated animals by behavioural tests, neuroimaging, biomarkers in blood and cerebrospinal fluid, and neuropathological analyses.

Tiberiu Loredan Stan

 
Working Experience

December 2014- present

Postdoctocroral Researcher, QPS Austria

2010 –2014

PhD (partly funded by Marie Curie fellowship)
Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden

2005 - 2008

Research assistant
Institute for Neurophysiology and Pathophysiology, University Medical Centre
Hamburg - Eppendorf, Hamburg, Germany

Education

2003 - 2005

MSc Neuroscience
Department of Neurobiology and Biophysics,
Faculty of Biology, University of Bucharest (Romania)

Institute for Neurophysiology and Pathophysiology, University Medical Centre
Hamburg - Eppendorf, Hamburg, Germany

Department of Neurobiology and Biophysics,
Faculty of Biology, University of Bucharest (Romania)

1999 - 2003

BSc Biology
Department of Biology, Faculty of Biology, University of Bucharest (Romania)

Work to be performed within SwitchHD:

1.

in vivo inactivation of mutant huntingtin (mHTT) in striatum and hypothalamus of BACHD rats by intrathecal administration of virus vector construct;

2.

further characterize the cognitive deficits and psychiatric symptoms of BACHD rats in different mazes setups;

3.

longitudinal CSF sampling, biochemical measurements in the CSF, blood and brain tissue;

4.

evaluating the effects of selectively inactivation of mHTT in striatum.

Libo Yu-Taeger

 
Work Experience

Jan.2014-present

Post-Doc in the Huntington Disease Research Group at the Institute of Medical Genetics and Applied Genomics, University of Tuebingen

Research topic: Neuropathogenesis of HD and Dystonia

Jul.2013-Dec.2013

Post-Doc at at QPS Austria GmbH

Research topic: Silencing transgene mutant huntingtin in BACHD rats using viral transduction to deliver recombinase Cre

Nov.2007-Jun.2013

Ph.D. candidate in the Huntington Disease Research Group at the Institute of Medical Genetics and Applied Genomics, University of Tuebingen

Research topic: Generation and Characterization of BACHD transgene rats expressing full-length human mutant huntingtin

Sep.2006-Oct.2007

Undergraduate student at Hertie-Institute for Clinical Brain Research, University of Tuebingen

Research topic: Aging’s effect on neurodegeneration processes in Alzheimer disease

Works performed for SWITCH-HD
1. Transferring knowledge to QPS regarding genotyping and handling of BACHD rats
2. Evaluation of transduction efficacy in vitro and in vivo in BACHD rats. For this work, Libo Yu-Taeger performed viral transduction using primary cortical neurons and intrastriatal injection in BACHD rats. Cre-mediated excision of floxed DNA sequence in the transgene mutant huntingtin (mHTT) was confirmed in vitro and in vivo. The transduction efficiency was investigated showing approximately 40% transduced cells in vitro and 5% in vivo. The expressions of mHTT on the RAN and protein levels were compared between viral transduced cells/striatum and the controls. Reduced mHTT expression was found in the viral transduced primary cortical neurons, while there was no difference of mHTT expression was detected in the viral injected striatum due to very low transduction efficiency in vivo
SwitchHD is funded from the European Community’s Seventh Framework Programme FP7/2012 under grant agreement No. 324495
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