Epilepsy, the most common neurological disorder, is characterized by seizures resulting from an imbalance between brain excitation and inhibition, leading to sudden neuronal hyperexcitability and synchronized brain activity. It can arise from various causes, including genetic, metabolic, infectious, structural, immune, and traumatic factors. Traditionally, treatments focus on ion channels and receptors in neurons; however, recent research highlights the role of astrocytes and microglia in epilepsy's pathophysiology.
Non-selective macro channels in neurons and glial cells, such as connexin43 (Cx43), pannexin1 (Panx1), and others, are implicated in epilepsy. Additionally, epilepsy is often associated with neuroinflammation, influenced by factors like etiology intensity, patient age, and more. Inflammation involves pro-inflammatory cytokine production in glial and myeloid cells, affecting seizure regions. These cytokines, produced by cells like mast cells and astrocytes, influence neurons and neurotransmitter production. Drug-resistant patients often have higher serum cytokine levels, which may worsen seizure susceptibility and brain dysfunction.
Despite the connections between inflammation and epilepsy, treatment rarely includes anti-inflammatory strategies, possibly affecting drug resistance. Recent experiments have shown that inhibiting certain macro channels reduces symptoms in models of epilepsy, suggesting inflammation's critical role. Understanding cellular mechanisms in epilepsy could lead to better treatments and improved patient quality of life.
This Research Topic highly welcomes original research articles, review manuscripts and methods articles covering, but not restricted to:
o Interconnection Between Inflammation and Epilepsy: Explore how inflammation acts as both a cause and effect of epileptic seizures.
o Mechanisms of Neuroinflammation: Investigate cellular and molecular mechanisms contributing to neuroinflammation in epilepsy.
o Role of Non-Neuronal Cells: Examine the involvement of astrocytes, microglia, and other glial cells in the pathophysiology of epilepsy.
o Impact of Cytokines: Assess how pro-inflammatory cytokines influence seizure susceptibility and treatment resistance
Topic Editor Chunyue Geoffrey Lau is the co-inventor of a patent, 一种半通道抑制剂在药学上的应用 / Pharmaceutical application of a hemichannel inhibitor (CityU KTO IDF: PWG/PA/1201/3/2022; application number: CN202211496351.7, 25 Nov, 2022; preliminarily approved, 16 Jan, 2023.) Public announcement number: CN 118078818 A (28 May, 2024). All other Topic Editors declare no conflicts of interest.
Keywords:
epilepsy, inflammation, physiology
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Epilepsy, the most common neurological disorder, is characterized by seizures resulting from an imbalance between brain excitation and inhibition, leading to sudden neuronal hyperexcitability and synchronized brain activity. It can arise from various causes, including genetic, metabolic, infectious, structural, immune, and traumatic factors. Traditionally, treatments focus on ion channels and receptors in neurons; however, recent research highlights the role of astrocytes and microglia in epilepsy's pathophysiology.
Non-selective macro channels in neurons and glial cells, such as connexin43 (Cx43), pannexin1 (Panx1), and others, are implicated in epilepsy. Additionally, epilepsy is often associated with neuroinflammation, influenced by factors like etiology intensity, patient age, and more. Inflammation involves pro-inflammatory cytokine production in glial and myeloid cells, affecting seizure regions. These cytokines, produced by cells like mast cells and astrocytes, influence neurons and neurotransmitter production. Drug-resistant patients often have higher serum cytokine levels, which may worsen seizure susceptibility and brain dysfunction.
Despite the connections between inflammation and epilepsy, treatment rarely includes anti-inflammatory strategies, possibly affecting drug resistance. Recent experiments have shown that inhibiting certain macro channels reduces symptoms in models of epilepsy, suggesting inflammation's critical role. Understanding cellular mechanisms in epilepsy could lead to better treatments and improved patient quality of life.
This Research Topic highly welcomes original research articles, review manuscripts and methods articles covering, but not restricted to:
o Interconnection Between Inflammation and Epilepsy: Explore how inflammation acts as both a cause and effect of epileptic seizures.
o Mechanisms of Neuroinflammation: Investigate cellular and molecular mechanisms contributing to neuroinflammation in epilepsy.
o Role of Non-Neuronal Cells: Examine the involvement of astrocytes, microglia, and other glial cells in the pathophysiology of epilepsy.
o Impact of Cytokines: Assess how pro-inflammatory cytokines influence seizure susceptibility and treatment resistance
Topic Editor Chunyue Geoffrey Lau is the co-inventor of a patent, 一种半通道抑制剂在药学上的应用 / Pharmaceutical application of a hemichannel inhibitor (CityU KTO IDF: PWG/PA/1201/3/2022; application number: CN202211496351.7, 25 Nov, 2022; preliminarily approved, 16 Jan, 2023.) Public announcement number: CN 118078818 A (28 May, 2024). All other Topic Editors declare no conflicts of interest.
Keywords:
epilepsy, inflammation, physiology
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.