The research at our departments focuses on the pathophysiology of epilepsy and epileptic seizures in adulthood and particularly in the developing brain. In our research we are utilizing modern electrophysiological, imaging, biochemical and pharmacological techniques. To elucidate the cellular and network mechanisms involved in epilepsy and to increase the translational potential of new observations we are using extensively chronic models of acquired epilepsy and also genetic models and also collaborate with leading epilepsy centres.
Our primary research topics are:
- Consequences of brain injury during early stages of the brain development
- Mechanisms responsible for seizure initiation and termination.
- Impact of seizures on the developing brain
- Development of new diagnostic techniques of epilepsy
- Cognitive and behavioural consequences of epilepsy
- The role of oxidative stress in pathogenesis of epilepsy and seizures during the development
- Impact of antiepileptic therapy of the brain development
- Age-specific mechanisms of seizure initiation and propagation
Projects
Brain-damaging insult triggers a cascade of molecular, cellular and structural changes that eventually lead to behavioral alterations and development of epilepsy. The response to the particular brain insult is highly age-dependent. Our aim is to study effects of early insults on the brain development at the molecular, cellular, and circuitry levels (maturation of receptors or ionic channel structures, vascularisation, myelination, circuitry maturation, etc.) and consequently on maturation of more complex brain functions (cognitive functions, sensorimotor skills, social and emotional behavior, brain excitability, etc.). Results of our research can be used to develop age specific pharmacological strategies for prevention of epilepsy development and disturbances of brain function.
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Systems important for brain excitability and its regulation mature for a long period of postnatal life.
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Period of perinatal and early postnatal development represents critical time for future brain functions and capabilities, as brain plasticity permits experiences to shape the immature brain.
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Oxidative stress and mitochondrial dysfunction are implicated in the pathogenesis of many neurological disorders, including epilepsy.
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Achievements
Epileptology European Award 2016 was awarded prof. Pavel Mareš.
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Publications
Tykalová, T. - Pospíšilová, M. - Čmejla, R. - Jeřábek, J. - Mareš, Pavel - Rusz, J.
Speech changes after coordinative training in patients with cerebellar ataxia: a pilot study
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Neurological Sciences. 2016, roč. 37, 2, p. 293-296
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IF = 1.783
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doi
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Mareš, Pavel - Kubová, Hana
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Does status epilepticus induced at early postnatal period change excitability after cortical epileptic afterdischarges?
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Epilepsia. 2016, roč. 57, 8, E183-E186
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IF = 4.706
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doi
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Kasal, Alexander - Buděšínský, Miloš - Mareš, Pavel - Krištofíková, Z. - Leitao, A. J. - Sá e Melo, M. L. - Silva, M. M. C.
Neurosteroids: Can a 2alpha,3alpha-epoxy ring make up for the 3alpha-hydroxyl group?
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Steroids. 2016, roč. 105, Jan, p. 12-18
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IF = 2.513
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doi
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Folbergrová, Jaroslava - Ješina, Pavel - Kubová, Hana - Druga, Rastislav - Otáhal, Jakub
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Status Epilepticus in Immature Rats Is Associated with Oxidative Stress and Mitochondrial Dysfunction
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Frontiers in Cellular Neuroscience. 2016, roč. 10, May 26, p. 136
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IF = 4.609
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doi
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Fábera, Petr - Krijtová, H. - Tomášek, M. - Krýsl, D. - Zámečník, J. - Mohapl, M. - Jiruška, Přemysl - Marusič, P.
Familial temporal lobe epilepsy due to focal cortical dysplasia type IIIa
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Seizure-European Journal of Epilepsy. 2015, Vol. 31, -, p. 120-123
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IF = 2.109
[ASEP]
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doi
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