Rita Horvath is a Director of Research in Genetics of Rare Neurological Disorders at the University of Cambridge and Honorary Consultant in Neurology. She trained as a neurologist in Budapest, Hungary and completed her PhD on mitochondrial disease. She started laboratory research in Eric Shoubridge`s laboratory at the Montreal Neurological Institute before working in mitochondrial laboratories of the Academic Hospital Schwabing and the Medical Genetic Center in Munich Germany from 1999 to 2007. She was later appointed as Lecturer in the Mitochondrial Research Group at Newcastle University, where she established her research group to study mitochondrial translation deficiencies and was promoted to Professor of Neurogenetics in 2013 in the Institute of Genetic Medicine as part of the Newcastle Wellcome Trust Centre for Mitochondrial Research. As a clinician, she developed a new service in Newcastle for patients with inherited peripheral neuropathies (Charcot-Marie-Tooth disease, CMT). In September 2018 Rita took on the post of Director of Research (Clinical) at the Department of Clinical Neurosciences, University of Cambridge. The focus of her research is identifying key molecular disease mechanisms with the aim of developing treatments for patients with rare inherited neurological conditions, such as mitochondrial disease and CMT.
Dr Horvath Laboratory
Rita Horvath’s laboratory research focusses on understanding the molecular mechanisms of tissue specific clinical presentations in some forms of mitochondrial diseases (abnormal mitochondrial protein synthesis), with the aim of developing treatments. They also study molecular mechanisms and clinical biomarkers in inherited peripheral neuropathies (Charcot-Marie-Tooth Disease). In the skeletal muscle and cells of patients with tissue specific mitochondrial diseases Dr Horvath’s group has identified some molecular targets which they continue to investigate in primary fibroblasts, myoblasts and iPSC-derived neurons and muscle cells. In parallel, the group also uses zebrafish models of mitochondrial diseases caused by abnormal mitochondrial translation or mtDNA depletion to study the effect of targeted treatments in transgenic zebrafish. Comparing the results in human cells and zebrafish will validate molecular targets, which can be further studied in the clinic.
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