Epileptogenesis can be defined as a process by which a normal brain develops epilepsy, and by which epilepsy worsens. Though already used in the early 1960s to describe cortical changes in experimental kindling models, we have recently witnessed a renaissance of research focus on epileptogenesis. This is mainly because all current pharmacological treatments only symptomatically suppress seizures, and do not tackle the underlying brain dysfunctions causing them. To cure or prevent epilepsy in the future we need to understand the mechanisms at play that promote the development or worsening of epilepsy. With our novel understanding of glial cells as major contributors to inflammation and brain excitability, as well as new technologies that allow improved investigation of the mechanisms of epileptogenesis, we are approaching novel curative treatment strategies for epilepsy.
We recently learned that glial cells acquire specific dysfunctional and reactive phenotypes in epileptic foci. Importantly, the acquisition of these altered properties begins very quickly after an initial epileptogenic event. Targeting dysfunctional and reactive glia or upstream inflammatory processes may thus prevent initiation and progression of epilepsy. However, the following questions must still be answered: What is the time course of these changes after an initial epileptogenic event like status epilepticus, febrile seizure, trauma or stroke? Do proinflammatory cytokines have a role in early astrocyte dysregulation, and which are the key players? Do changes in astrocyte metabolism contribute to epileptogenesis? What are the upstream mechanisms of epileptogenesis and are they detectable by means of studying epigenetics?
We also aim to better understand glial scar formation in various cerebral conditions associated with epilepsy like stroke, trauma, and complex febrile seizure, and to identify biomarkers of epilepsy progression in these conditions. We would also like to elucidate whether there is a specific time window for rescue or reversal of these changes. We would also like to touch on how the development of diagnostic tools for patient stratification, risk factor detection, and identification of reliable biomarkers of progression can further facilitate treatment and management of these disorders.
We welcome basic, translational and (pre)clinical research on all aspects of epileptogenesis, with special focus on the following areas:
• Studies highlighting in which ways dysfunction of glial cells and glia-neuron interplay promotes epileptogenesis.
• Deciphering upstream mechanisms, including epigenetic changes, during the process of epilepsy development.
• Identification of diagnostic tools, biomarkers and risk factors of epileptogenesis.
• Studies on inflammation-induced glial dysfunction that promotes neuronal excitability and epileptogenesis.
• Studies on novel targets and substrates disrupting or reversing epileptogenesis.
Epileptogenesis can be defined as a process by which a normal brain develops epilepsy, and by which epilepsy worsens. Though already used in the early 1960s to describe cortical changes in experimental kindling models, we have recently witnessed a renaissance of research focus on epileptogenesis. This is mainly because all current pharmacological treatments only symptomatically suppress seizures, and do not tackle the underlying brain dysfunctions causing them. To cure or prevent epilepsy in the future we need to understand the mechanisms at play that promote the development or worsening of epilepsy. With our novel understanding of glial cells as major contributors to inflammation and brain excitability, as well as new technologies that allow improved investigation of the mechanisms of epileptogenesis, we are approaching novel curative treatment strategies for epilepsy.
We recently learned that glial cells acquire specific dysfunctional and reactive phenotypes in epileptic foci. Importantly, the acquisition of these altered properties begins very quickly after an initial epileptogenic event. Targeting dysfunctional and reactive glia or upstream inflammatory processes may thus prevent initiation and progression of epilepsy. However, the following questions must still be answered: What is the time course of these changes after an initial epileptogenic event like status epilepticus, febrile seizure, trauma or stroke? Do proinflammatory cytokines have a role in early astrocyte dysregulation, and which are the key players? Do changes in astrocyte metabolism contribute to epileptogenesis? What are the upstream mechanisms of epileptogenesis and are they detectable by means of studying epigenetics?
We also aim to better understand glial scar formation in various cerebral conditions associated with epilepsy like stroke, trauma, and complex febrile seizure, and to identify biomarkers of epilepsy progression in these conditions. We would also like to elucidate whether there is a specific time window for rescue or reversal of these changes. We would also like to touch on how the development of diagnostic tools for patient stratification, risk factor detection, and identification of reliable biomarkers of progression can further facilitate treatment and management of these disorders.
We welcome basic, translational and (pre)clinical research on all aspects of epileptogenesis, with special focus on the following areas:
• Studies highlighting in which ways dysfunction of glial cells and glia-neuron interplay promotes epileptogenesis.
• Deciphering upstream mechanisms, including epigenetic changes, during the process of epilepsy development.
• Identification of diagnostic tools, biomarkers and risk factors of epileptogenesis.
• Studies on inflammation-induced glial dysfunction that promotes neuronal excitability and epileptogenesis.
• Studies on novel targets and substrates disrupting or reversing epileptogenesis.
