Tibor Harkany Group
Tibor Harkany's profile page.
Principal Investigator’s Brief Profile
Tibor Harkany completed his undergraduate training (M.Sci.) in molecular biology and biotechnology at University of Szeged, Hungary (1995). He was awarded Ph.D. in Medical Sciences from Semmelweis University (Budapest, Hungary; 1999) for his studies on the neurotoxicity of β-amyloid peptides and their relevance to cholinergic neurodegeneration in Alzheimer’s disease. Two post-doctoral fellowships ensued (University of Groningen, Netherlands; 1999-2001, Karolinska Institutet; 2002-2004), the latter supported by a “Karolinska Institute postgraduate fellowship in restorative neuroscience”.
In 2005, Tibor Harkany formed his independent research group at the Department of Medical Biochemistry & Biophysics. This year saw him to receive his associate professorship (“docentship”) in neuropharmacology. During 2007-2013, Dr. Harkany held the post of SULSA Professor and 6th Century Chair of Cell Biology at the University of Aberdeen in Scotland. Since 2011, he is Professor of Neurobiology at Karolinska Institutet, a role he maintains besides his appointment at the Medical University of Vienna.
Dr Harkany was elected as a member of the European Molecular Biology Organization’s Young investigator Program (2007) and fellow of the Society of Biology (FSB, 2010). He also received the Anders Jahre (2012), ICAM (2013) and Erik K. Fernström (2013) prizes for young scientists.
The Harkany group carries out frontier and multidisciplinary research, primarily focusing on the following topics:
- Endocannabinoid signaling in the developing nervous system,
- Molecular mechanisms of psychoactive drug action in the fetal brain,
- Calcium-binding protein functions in the nervous system, with particular emphasis on hypothalamic neuropeptide and hormone release,
- Molecular identity of sensory and hypothalamic neurons.
Endocannabinoid signaling during neuronal development
During the recent past, significant research activity was dedicated towards understanding the system-level, cellular and molecular organization of endocannabinoid signaling networks in the developing cerebral cortex. These studies identified endocannabinoids as axon guidance cues, and demonstrated that sub-cellular enzymatic arrangements for endocannabinoid metabolism are such that endocannabinoid signals focus in growth cones, allowing for an autocrine action for these bioactive lipids. Notably, these molecular studies also suggested that BRCA1 is a candidate ubiquitin ligase involved in determining the turnover of monoacylglycerol lipase, a rate-limiting enzyme of endocannabinoid degradation. In addition, a combination of unbiased proteomics, mouse genetics and molecular pharmacology studies demonstrated that THC from Cannabis spp. impairs synaptic organization of the cerebral cortex by modifying cytoskeletal instability. In particular, SCG10/brain-specific stathmin-2 was identified as a key molecular target downstream from CB1 cannabinoid receptors.
Calcium sensor proteins in the nervous system
Another line of research is aimed at identifying novel calcium-binding proteins (particularly sensors) in the central nervous system. A prime example is secretagogin, which is expressed during embryonic development, localizes to migrating neuronal contingents, which mature into specific and distinct subtypes of olfactory, amygdala, hippocampal and hypothalamic neurons. Recent data show that secretagogin's calcium-sensor function is required for the molecular control of CRH release in the hypothalamus upon acute stress. These studies, also combining single cell transcriptome analysis with unbiased proteomics, defined a hitherto unknown population of parvocellular neurons in the paraventricular nucleus of the hypothalamus controlling the induction of the HPA axis upon acute stress.
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