Epilepsy is a neurological disorder causing spontaneous seizures because of abnormal brain activities. There is a meaningful connection between epilepsy and the immune system as neuroinflammation and an increase in the permeability of the blood-brain barrier (BBB) are the hallmark of this disorder. Moreover, toll-like receptors (TLRs), which are one of the tools of the innate immune system, have been shown to be associated with epileptogenesis as well as infiltration of T-cell lymphocytes to the brain in different types of epileptic disorders, which is indicative of the involvement of adaptive immunity. Most of the antiepileptic drugs do not modify the immune system and act on excitatory or inhibitory neurotransmission in the brain.
Refractory epilepsy occurs in approximately one-third of patients; therefore, discovering a novel class of antiepileptic medications is imperative. To pursue that goal, we need to comprehensively understand the pathophysiology of epilepsy. Although the involvement of the immune system has been established in epileptogenesis and spontaneous seizures, the mechanisms by which the immune system impacts them are abstruse. Recently, there has been a shift in the literature to unveil immune-related processes in glial cells and migrated immune cells, contributing to seizures; nevertheless, the connection between them and neurons is elusive. For example, one study showed that activation of TLR-4 in astrocytes increases excitatory synaptogenesis through extracellular signal–regulated kinase 1/2 downstream, however, it failed to explain the process that transpired in neurons to cause the synaptogenesis. By understanding the pathways employed by the immune system in epilepsy, we will have a much better chance to discover a new class of medications and we can decrease the number of patients with refractory epilepsy.
In this Research Topic we are going to look at the immune system-related pathways involved in epileptogenesis and spontaneous seizures. This will include the following themes:
• The role of both innate and adaptive immunity on the onset of epilepsy
• different etiology especially how different lines of immunity contribute to the first seizure.
• How do glial cells affect neurons in an epileptic brain?
• Pathways by which glial cells or migrated immune cells employ to impact neurons
• Pathways activated or deactivated in neurons which lead to seizure behavior
• What is the most effective way to tackle the involvement of the immune system? Is there a specific target?
• The effect of the BBB disruption on epilepsy. Is it the cause or a symptom?
• Does improving the BBB disruption reduce seizure frequency in all types of epilepsy?
Topic Editor Dr. Yi Li declares that she receives research support from the Stanford Maternal and Child Health Research Institute, and American Epilepsy Society. Additionally, she serves on the uniQure Advisory Board. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Epilepsy is a neurological disorder causing spontaneous seizures because of abnormal brain activities. There is a meaningful connection between epilepsy and the immune system as neuroinflammation and an increase in the permeability of the blood-brain barrier (BBB) are the hallmark of this disorder. Moreover, toll-like receptors (TLRs), which are one of the tools of the innate immune system, have been shown to be associated with epileptogenesis as well as infiltration of T-cell lymphocytes to the brain in different types of epileptic disorders, which is indicative of the involvement of adaptive immunity. Most of the antiepileptic drugs do not modify the immune system and act on excitatory or inhibitory neurotransmission in the brain.
Refractory epilepsy occurs in approximately one-third of patients; therefore, discovering a novel class of antiepileptic medications is imperative. To pursue that goal, we need to comprehensively understand the pathophysiology of epilepsy. Although the involvement of the immune system has been established in epileptogenesis and spontaneous seizures, the mechanisms by which the immune system impacts them are abstruse. Recently, there has been a shift in the literature to unveil immune-related processes in glial cells and migrated immune cells, contributing to seizures; nevertheless, the connection between them and neurons is elusive. For example, one study showed that activation of TLR-4 in astrocytes increases excitatory synaptogenesis through extracellular signal–regulated kinase 1/2 downstream, however, it failed to explain the process that transpired in neurons to cause the synaptogenesis. By understanding the pathways employed by the immune system in epilepsy, we will have a much better chance to discover a new class of medications and we can decrease the number of patients with refractory epilepsy.
In this Research Topic we are going to look at the immune system-related pathways involved in epileptogenesis and spontaneous seizures. This will include the following themes:
• The role of both innate and adaptive immunity on the onset of epilepsy
• different etiology especially how different lines of immunity contribute to the first seizure.
• How do glial cells affect neurons in an epileptic brain?
• Pathways by which glial cells or migrated immune cells employ to impact neurons
• Pathways activated or deactivated in neurons which lead to seizure behavior
• What is the most effective way to tackle the involvement of the immune system? Is there a specific target?
• The effect of the BBB disruption on epilepsy. Is it the cause or a symptom?
• Does improving the BBB disruption reduce seizure frequency in all types of epilepsy?
Topic Editor Dr. Yi Li declares that she receives research support from the Stanford Maternal and Child Health Research Institute, and American Epilepsy Society. Additionally, she serves on the uniQure Advisory Board. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
