School of Biomedicine
Faculty of Health and Medical Sciences
Dr Stefka Mincheva Tasheva
2017 Postdoctoral Research Fellow University of Adelaide, Adelaide
2015 - 2016 Postdoctoral Research Fellow University of Queensland, Brisbane
2011 - 2014 Postdoctoral Research Fellow University of Lleida, Spain.
Neuroscience, Behaviour and Brain Health Cell Biology Cell Development, Proliferation and Death Cellular Nervous System Central Nervous System Peripheral Nervous System
Dr. Stefka Mincheva-Tasheva is a postdoctoral researcher in Prof. Paul Thomas’ Genome Editing laboratory at The University of Adelaide. Her research interest and expertise centers around the identification and characterisation of the molecular mechanisms governing physiological processes during nervous system development and disease.
Dr. Tasheva completed her Ph.D. in Health Sciences in 2011 at the University of Lleida (UdL), Spain. Her dissertation explored the signalling pathways controlling motor neuron survival during spinal cord development and in Spinal Muscular Atrophy. During her first postdoctoral training at UdL, she contributed to the characterisation of the molecular basis for Friedreich ataxia (FRDA) and discovered a new therapeutic target to restore the symptoms of this progressive disease. Then Stefka undertook a second post-doctoral position at The University of Queensland where she investigated the role of cellular tight junctions in Type II Diabetes.
Dr. Tasheva joined Prof. Thomas’ lab in 2017 and her ongoing research expands on animal disease modelling for identification of the molecular mechanism and therapeutic strategies for a very intriguing epileptic syndrome called PCDH19-Clustering Epilepsy (PCDH19-CE). The objective of her project is to investigate the possibilities for using gene therapy to treat the disease. To this end, she together with Prof. Thomas have developed a unique Pcdh19 mouse model that mimics the genetic changes that cause epilepsy. Using this pre-clinical model, she is working to identify when pathological changes first occur in the brain of the affected females and whether these lesions are reversible and, if so, the latest developmental time point by which genetic intervention must occur.
Date Position Institution name 2017 - ongoing Postdoctoral Research Fellow University of Adelaide, Adelaide 2015 - 2016 Postdoctoral Research Fellow University of Queensland, Brisbane 2011 - 2014 Postdoctoral Research Fellow University of Lleida, Lleida
Date Institution name Country Title 2006 - 2011 University of Lleida Spain PhD in Health Sciences
Year Citation 2021 Tasheva, S., Nieto Guil, A. F., Homan, C. C., Gecz, J., & Thomas, P. Q. (2021). Disrupted excitatory synaptic contacts and altered neuronal network activity underpins the neurological phenotype in PCDH19-clustering epilepsy (PCDH19-CE). Molecular Neurobiology, 58(5), 2005-2018.
DOI Scopus9 WoS9 Europe PMC7
2021 Britti, E., Delaspre, F., Sanz-Alcázar, A., Medina-Carbonero, M., Llovera, M., Purroy, R., . . . Ros, J. (2021). Calcitriol increases frataxin levels and restores mitochondrial function in cell models of Friedreich Ataxia. Biochemical Journal, 478(1), 1-20.
DOI Scopus3 Europe PMC1
2018 Arumugam, S., Mincheva-Tasheva, S., Periyakaruppiah, A., de la Fuente, S., Soler, R., & Garcera, A. (2018). Regulation of Survival Motor Neuron Protein by the Nuclear Factor-Kappa B Pathway in Mouse Spinal Cord Motoneurons. Molecular Neurobiology, 55(6), 5019-5030.
DOI Scopus9 Europe PMC5
2018 Pederick, D., Richards, K., Piltz, S., Kumar, R., Mincheva-Tasheva, S., Mandelstam, S., . . . Thomas, P. (2018). Abnormal cell sorting underlies the unique X-linked inheritance of PCDH19 epilepsy. Neuron, 97(1), 59-e5.
DOI Scopus62 WoS61 Europe PMC40
2014 Mincheva-Tasheva, S., Obis, E., Tamarit, J., & Ros, J. (2014). Apoptotic cell death and altered calcium homeostasis caused by frataxin depletion in dorsal root ganglia neurons can be prevented by BH4 domain of Bcl-xL protein. Human Molecular Genetics, 23(7), 1829-1841.
DOI Scopus39 Europe PMC30
2013 Mincheva-Tasheva, S., & Soler, R. M. (2013). NF-κB signaling pathways: Role in nervous system physiology and pathology. Neuroscientist, 19(2), 175-194.
DOI Scopus95 Europe PMC61
2011 Mincheva, S., Garcera, A., Gou-Fabregas, M., Encinas, M., Dolcet, X., & Soler, R. M. (2011). The canonical nuclear factor-κB pathway regulates cell survival in a developmental model of spinal cord motoneurons. Journal of Neuroscience, 31(17), 6493-6503.
DOI Scopus19 Europe PMC15
2011 Garcera, A., Mincheva, S., Gou-Fabregas, M., Caraballo-Miralles, V., Lladó, J., Comella, J. X., & Soler, R. M. (2011). A new model to study spinal muscular atrophy: Neurite degeneration and cell death is counteracted by BCL-XL Overexpression in motoneurons. Neurobiology of Disease, 42(3), 415-426.
DOI Scopus26 Europe PMC25
2009 Gou-Fabregas, M., Garcera, A., Mincheva, S., Perez-Garcia, M. J., Comella, J. X., & Soler, R. M. (2009). Specific vulnerability of mouse spinal cord motoneurons to membrane depolarization. Journal of Neurochemistry, 110(6), 1842-1854.
DOI Scopus19 Europe PMC18
Title: Investigating the molecular pathology for PCDH19-Girls Clustering Epilepsy
Funding scheme: FND000667: NHMRC-Ideas Grants
Description: Changes in the PCDH19 gene are a relatively common cause of epilepsy. To better understand the basis of this disorder, we will use mouse models that mimic the genetic changes and symptoms of PCDH19-GCE. We will perform careful analysis of brain development in these models to determine the primary cause of this condition. We will also test whether gene therapy could be used to cure the disease. This study will define how brain changes lead to epilepsy and facilitate development of new treatments.
Funder name: National Health and Medical Research Council
Investigators: Thomas P; Tasheva S
Reporting dates: 01 Jan 2020 to 31 Dec 2023
Title: Exploring proof of concept for genetic therapy of PCDH19-girls clustering epilepsy using preclinical models
Funding scheme: ORG120981: PCDH19 Alliance Research Grant
Description: Changes in a brain gene called PCDH19 are a relatively common cause of epilepsy with intellectual disability. An unusual feature of this condition is that genetic changes in PCDH19 affect girls while male carriers are spared. It is thought that mosaic activity of the PCDH19 gene (coexistence of PCDH19-expressing and -null cells) in the developing brain is the cause of the disease pathology. There is no current cure for the disorder and more than half of the patients do not respond to anti-epileptic drugs. The aim of this project is to investigate the possibilities for using gene therapy to treat the disease. PCDH19-GCE is an excellent candidate for gene eliminating strategies because uniformly null individuals are not affected. To this end, we have developed a unique Pcdh19 mouse model that mimics the genetic changes that cause epilepsy. Using this pre-clinical model we will identify when pathological changes first occur in the brain of the affected females. Importantly, we will also determine whether the pathological lesion is reversible and, if so, the latest developmental time point by which genetic intervention must occur. These unique experiments will provide unique insight into PCDH19 pathology and demonstrate for the first time whether it might be possible to cure PCDH19-GCE using genetic intervention.
Funder name: PCDH19 Alliance
Investigators: Thomas P; Tasheva S
Reporting dates: 01 Sep 2019 to 01 Sep 2020
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