Stefka Tasheva
School of Biomedicine
Faculty of Health and Medical Sciences
Eligible to supervise Masters and PhD (as Co-Supervisor) - email supervisor to discuss availability.
Dr Stefka Mincheva Tasheva
2017-present NHMRC Grant-Funded Researcher A, University of Adelaide
2015 - 2016 Postdoctoral Research Fellow, University of Queensland, Brisbane
2011 - 2014 Postdoctoral Research Fellow, University of Lleida, Spain.
Research Interests:
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 the 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 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's work at the University of Adelaide is centred on animal disease modelling and therapeutic strategies for PCDH19-clustering epilepsy (PCDH19-CE). Over the past seven years, she has extensively studied the underlying causes of PCDH19-CE neuropathology and explored the role of PCDH19 in central nervous system function and dysfunction. Her current focus is on developing innovative gene therapy approaches with potential for clinical translation to treat this complex epileptic disorder. In addition to her work on gene therapy, Dr. Tasheva is pioneering research into a novel, non-invasive technique for delivering therapeutic agents to the brain.
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Appointments
Date Position Institution name 2017 - ongoing NHMRC Grant-Funded Researcher A, University of Adelaide, Adelaide 2015 - 2016 Postdoctoral Research Fellow University of Queensland, Brisbane 2011 - 2014 Postdoctoral Research Fellow University of Lleida, Lleida -
Language Competencies
Language Competency Bulgarian Can read, write, speak, understand spoken and peer review English Can read, write, speak, understand spoken and peer review Russian Can read, write, understand spoken and peer review Spanish; Castilian Can read, write, speak, understand spoken and peer review -
Education
Date Institution name Country Title 2006 - 2011 University of Lleida Spain PhD in Health Sciences -
Research Interests
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Journals
Year Citation 2024 de Nys, R., Gardner, A. E., van Eyk, C., Tasheva, S., Thomas, P. Q., Bhattacharjee, R., . . . Gecz, J. (2024). Proteomic analysis of the developing mammalian brain links PCDH19 to the Wnt/β-catenin signalling pathway. Molecular Psychiatry, 29(7), 2199-2210.
Scopus3 Europe PMC12024 Mincheva-Tasheva, S., Pfitzner, C., Kumar, R., Kurtsdotter, I., Scherer, M., Ritchie, T., . . . Thomas, P. Q. (2024). Mapping combinatorial expression of non-clustered protocadherins in the developing brain identifies novel PCDH19-mediated cell adhesion properties. Open Biology, 14(4), 230383-1-230383-13.
Europe PMC12021 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.
Scopus20 WoS14 Europe PMC172021 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.
Scopus15 WoS5 Europe PMC112018 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.
Scopus13 WoS12 Europe PMC92018 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.
Scopus97 WoS71 Europe PMC862014 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.
Scopus53 WoS46 Europe PMC482013 Mincheva-Tasheva, S., & Soler, R. M. (2013). NF-κB signaling pathways: Role in nervous system physiology and pathology. Neuroscientist, 19(2), 175-194.
Scopus121 WoS99 Europe PMC812011 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.
Scopus23 WoS23 Europe PMC202011 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.
Scopus31 WoS32 Europe PMC322009 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.
Scopus24 WoS23 Europe PMC24 -
Preprint
Year Citation 2024 Mincheva-Tasheva, S., Scherer, M., Robertson, L., Piltz, S., Bensalem, J., Pederick, D., & Thomas, P. (2024). Functional analysis of the epilepsy gene Pcdh19 using a novel GFP-reporter mouse model.
DOI2020 Britti, E., Delaspre, F., Medina-Carbonero, M., Sanz, A., Llovera, M., Purroy, R., . . . Ros, J. (2020). Calcitriol increases frataxin levels and restores altered markers in cell models of Friedreich Ataxia.
DOI
Title: A Novel In Utero Gene Therapy Strategy to Prevent Neuropathology in PCDH19 Clustering Epilepsy
Funding scheme: Lloyd Cox O&G Research Fund – 2025 People Support Scheme ($115K)
Investigator: Stefka Tasheva
Reporting Dates: 01 Jan 2025 - 31 Dec 2025
Description: My research aims to develop a novel in utero gene therapy strategy to prevent the pathological consequences of PCDH19 girls clustering epilepsy. This research represents an exploration of transplacental gene delivery, a field still in its early stages but with immense potential to transform the treatment of genetic neurodevelopmental disorders.
Title: Genetic therapy- a battle against PCDH19-Clustering Epilepsy
Funding scheme: FND001545: PCDH19 Syndrome Research Grants, Italy ($163K)
Investigators: co-PI
Reporting dates: Oct 2023 to Oct 2025
Description: Our research project aims to develop innovative treatment strategies for PCDH19-Clustering Epilepsy (PCDH19-CE). T To develop new treatments for PCDH19-CE, we need to understand when and how brain development is altered in affected individuals. Using this information, we aim to test a new treatment strategy for PCDH19-CE based on elimination of the causative gene. These studies will provide a platform to develop new therapeutic options for patients with PCDH19-CE. Ultimately, our research has the potential to revolutionize the treatment landscape for this disease, offering hope for improved outcomes and a better quality of life for affected individuals.
Title: Investigating proof-of-concept for genetic therapy of PCDH19-Clustering Epilepsy using preclinical mouse models
Funding Scheme: Channel 7 Children's Research Foundation ($100K)
Investigators: co-PI
Reporting dates: 2024-2025
Travel Grant Award S.Tasheva ($1200)
Funder Name: Faculty of Health and Medical Sciences (School of Biomedicine), The University of Adelaide
Reporting Dates: Feb 2024
Travel Award S.Tasheva ($2600)
Funder Name: School of Biomedicine, The University of Adelaide
Reporting Dates: Sep 2023
Research Travel Award S.Tasheva ($3000)
Funder Name: Faculty of Health and Medical Science, University of Adelaide
Reporting Dates: May 2023
Title: Investigating the molecular pathology for PCDH19-Girls Clustering Epilepsy
Funding scheme: FND000667: National Health and Medical Research Council -Ideas Grants ($935K)
Investigators: CIB
Reporting dates: 01 Jan 2020 to 31 Dec 2023
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. This study will define how brain changes lead to epilepsy and facilitate development of new treatments.
Title: Exploring proof of concept for genetic therapy of PCDH19-girls clustering epilepsy using preclinical models
Funding scheme: ORG120981: PCDH19 Alliance Research Grant, USA ($110K)
Investigators: co-PI
Reporting dates: 01 Sep 2019 to 01 Sep 2020
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. 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.
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