Can glial cells save neurons in epilepsy?
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Epilepsy is a neurological disorder caused by the pathological hyper-synchronization of neuronal discharges. The fundamental research of epilepsy mechanisms and the targets of drug design options for its treatment have focused on neurons. However, approximately 30% of patients suffering from epilepsy show resistance to standard anti-epileptic chemotherapeutic agents while the symptoms of the remaining 70% of patients can be alleviated but not completely removed by the current medications. Thus, new strategies for the treatment of epilepsy are in urgent demand. Over the past decades, with the increase in knowledge on the role of glia in the genesis and development of epilepsy, glial cells are receiving renewed attention. In a normal brain, glial cells maintain neuronal health and in partnership with neurons regulate virtually every aspect of brain function. In epilepsy, however, the supportive roles of glial cells are compromised, and their interaction with neurons is altered, which dis...rupts brain function. In this review, we will focus on the role of glia-related processes in epileptogenesis and their contribution to abnormal neuronal activity, with the major focus on the dysfunction of astroglial potassium channels, water channels, gap junctions, glutamate transporters, purinergic signaling, synaptogenesis, on the roles of microglial inflammatory cytokines, microglia-astrocyte interactions in epilepsy, and on the oligodendroglial potassium channels and myelin abnormalities in the epileptic brain. These recent findings suggest that glia should be considered as the promising next-generation targets for designing anti-epileptic drugs that may improve epilepsy and drug-resistant epilepsy.
Кључне речи:
astrocyte / cytokines / glutamate / ion channel / microglia / myelin / neuron / oligodendrocyte / purinergic signaling / seizuresИзвор:
NEURAL REGENERATION RESEARCH, 2023, 18, 7, 1417-1422Издавач:
- Wolters Kluwer – Medknow
Финансирање / пројекти:
- Grants from European Commission (H2020 MSCA-ITN EU-GliaPhD No. 72205)
- Agence Nationale de la Recherche, Nos. ANR-19-CE16-0018-03 and ANR-20CE16-0003-02
- Grants from Science and Technology Department of Zhejiang Province, China, No. 2021RC051
- Scientific Research Foundation for Returned Scholars of Hangzhou City, China, No. 2019
- Министарство науке, технолошког развоја и иновација Републике Србије, институционално финансирање - 200007 (Универзитет у Београду, Институт за биолошка истраживања 'Синиша Станковић') (RS-MESTD-inst-2020-200007)
- Министарство науке, технолошког развоја и иновација Републике Србије, институционално финансирање - 200053 (Универзитет у Београду, Институт за мултидисциплинарна истраживања) (RS-MESTD-inst-2020-200053)
Напомена:
- kategorija casopsisa M21
Институција/група
Institut za multidisciplinarna istraživanjaTY - JOUR AU - SHEN, Weida AU - Bogdanović Pristov, Jelena AU - Nobili, Paola AU - Nikolic, Ljiljana PY - 2023 UR - http://rimsi.imsi.bg.ac.rs/handle/123456789/2004 AB - Epilepsy is a neurological disorder caused by the pathological hyper-synchronization of neuronal discharges. The fundamental research of epilepsy mechanisms and the targets of drug design options for its treatment have focused on neurons. However, approximately 30% of patients suffering from epilepsy show resistance to standard anti-epileptic chemotherapeutic agents while the symptoms of the remaining 70% of patients can be alleviated but not completely removed by the current medications. Thus, new strategies for the treatment of epilepsy are in urgent demand. Over the past decades, with the increase in knowledge on the role of glia in the genesis and development of epilepsy, glial cells are receiving renewed attention. In a normal brain, glial cells maintain neuronal health and in partnership with neurons regulate virtually every aspect of brain function. In epilepsy, however, the supportive roles of glial cells are compromised, and their interaction with neurons is altered, which disrupts brain function. In this review, we will focus on the role of glia-related processes in epileptogenesis and their contribution to abnormal neuronal activity, with the major focus on the dysfunction of astroglial potassium channels, water channels, gap junctions, glutamate transporters, purinergic signaling, synaptogenesis, on the roles of microglial inflammatory cytokines, microglia-astrocyte interactions in epilepsy, and on the oligodendroglial potassium channels and myelin abnormalities in the epileptic brain. These recent findings suggest that glia should be considered as the promising next-generation targets for designing anti-epileptic drugs that may improve epilepsy and drug-resistant epilepsy. PB - Wolters Kluwer – Medknow T2 - NEURAL REGENERATION RESEARCH T1 - Can glial cells save neurons in epilepsy? EP - 1422 IS - 7 SP - 1417 VL - 18 DO - 10.4103/1673-5374.360281 ER -
@article{ author = "SHEN, Weida and Bogdanović Pristov, Jelena and Nobili, Paola and Nikolic, Ljiljana", year = "2023", abstract = "Epilepsy is a neurological disorder caused by the pathological hyper-synchronization of neuronal discharges. The fundamental research of epilepsy mechanisms and the targets of drug design options for its treatment have focused on neurons. However, approximately 30% of patients suffering from epilepsy show resistance to standard anti-epileptic chemotherapeutic agents while the symptoms of the remaining 70% of patients can be alleviated but not completely removed by the current medications. Thus, new strategies for the treatment of epilepsy are in urgent demand. Over the past decades, with the increase in knowledge on the role of glia in the genesis and development of epilepsy, glial cells are receiving renewed attention. In a normal brain, glial cells maintain neuronal health and in partnership with neurons regulate virtually every aspect of brain function. In epilepsy, however, the supportive roles of glial cells are compromised, and their interaction with neurons is altered, which disrupts brain function. In this review, we will focus on the role of glia-related processes in epileptogenesis and their contribution to abnormal neuronal activity, with the major focus on the dysfunction of astroglial potassium channels, water channels, gap junctions, glutamate transporters, purinergic signaling, synaptogenesis, on the roles of microglial inflammatory cytokines, microglia-astrocyte interactions in epilepsy, and on the oligodendroglial potassium channels and myelin abnormalities in the epileptic brain. These recent findings suggest that glia should be considered as the promising next-generation targets for designing anti-epileptic drugs that may improve epilepsy and drug-resistant epilepsy.", publisher = "Wolters Kluwer – Medknow", journal = "NEURAL REGENERATION RESEARCH", title = "Can glial cells save neurons in epilepsy?", pages = "1422-1417", number = "7", volume = "18", doi = "10.4103/1673-5374.360281" }
SHEN, W., Bogdanović Pristov, J., Nobili, P.,& Nikolic, L.. (2023). Can glial cells save neurons in epilepsy?. in NEURAL REGENERATION RESEARCH Wolters Kluwer – Medknow., 18(7), 1417-1422. https://doi.org/10.4103/1673-5374.360281
SHEN W, Bogdanović Pristov J, Nobili P, Nikolic L. Can glial cells save neurons in epilepsy?. in NEURAL REGENERATION RESEARCH. 2023;18(7):1417-1422. doi:10.4103/1673-5374.360281 .
SHEN, Weida, Bogdanović Pristov, Jelena, Nobili, Paola, Nikolic, Ljiljana, "Can glial cells save neurons in epilepsy?" in NEURAL REGENERATION RESEARCH, 18, no. 7 (2023):1417-1422, https://doi.org/10.4103/1673-5374.360281 . .