TY  - 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 . .

TY  - JOUR
AU  - Nobili, Paola
AU  - SHEN, Weida
AU  - Milicevic, Katarina
AU  - Bogdanović Pristov, Jelena
AU  - Audinat, Etienne
AU  - Nikolic, Ljiljana
PY  - 2022
UR  - http://rimsi.imsi.bg.ac.rs/handle/123456789/1813
AB  - Epilepsy and multiple sclerosis (MS), two of the most common neurological diseases, are
characterized by the establishment of inflammatory environment in the central nervous
system that drives disease progression and impacts on neurodegeneration. Current
therapeutic approaches in the treatments of epilepsy and MS are targeting neuronal
activity and immune cell response, respectively. However, the lack of fully efficient
responses to the available treatments obviously shows the need to search for novel
therapeutic candidates that will not exclusively target neurons or immune cells.
Accumulating knowledge on epilepsy and MS in humans and analysis of relevant
animal models, reveals that astrocytes are promising therapeutic candidates to target
as they participate in the modulation of the neuroinflammatory response in both diseases
from the initial stages and may play an important role in their development. Indeed,
astrocytes respond to reactive immune cells and contribute to the neuronal hyperactivity in
the inflamed brain. Mechanistically, these astrocytic cell to cell interactions are
fundamentally mediated by the purinergic signalling and involve metabotropic P2Y1
receptors in case of astrocyte interactions with neurons, while ionotropic P2X7
receptors are mainly involved in astrocyte interactions with autoreactive immune cells.
Herein, we review the potential of targeting astrocytic purinergic signalling mediated by
P2Y1 and P2X7 receptors to develop novel approaches for treatments of epilepsy and MS
at very early stages.
PB  - Frontiers Media
T2  - Frontiers in Pharmacology
T1  - Therapeutic Potential of Astrocyte Purinergic Signalling in Epilepsy and Multiple Sclerosis
SP  - 900337
VL  - 13
DO  - 10.3389/fphar.2022.900337
ER  - 

@article{
author = "Nobili, Paola and SHEN, Weida and Milicevic, Katarina and Bogdanović Pristov, Jelena and Audinat, Etienne and Nikolic, Ljiljana",
year = "2022",
abstract = "Epilepsy and multiple sclerosis (MS), two of the most common neurological diseases, are
characterized by the establishment of inflammatory environment in the central nervous
system that drives disease progression and impacts on neurodegeneration. Current
therapeutic approaches in the treatments of epilepsy and MS are targeting neuronal
activity and immune cell response, respectively. However, the lack of fully efficient
responses to the available treatments obviously shows the need to search for novel
therapeutic candidates that will not exclusively target neurons or immune cells.
Accumulating knowledge on epilepsy and MS in humans and analysis of relevant
animal models, reveals that astrocytes are promising therapeutic candidates to target
as they participate in the modulation of the neuroinflammatory response in both diseases
from the initial stages and may play an important role in their development. Indeed,
astrocytes respond to reactive immune cells and contribute to the neuronal hyperactivity in
the inflamed brain. Mechanistically, these astrocytic cell to cell interactions are
fundamentally mediated by the purinergic signalling and involve metabotropic P2Y1
receptors in case of astrocyte interactions with neurons, while ionotropic P2X7
receptors are mainly involved in astrocyte interactions with autoreactive immune cells.
Herein, we review the potential of targeting astrocytic purinergic signalling mediated by
P2Y1 and P2X7 receptors to develop novel approaches for treatments of epilepsy and MS
at very early stages.",
publisher = "Frontiers Media",
journal = "Frontiers in Pharmacology",
title = "Therapeutic Potential of Astrocyte Purinergic Signalling in Epilepsy and Multiple Sclerosis",
pages = "900337",
volume = "13",
doi = "10.3389/fphar.2022.900337"
}

Nobili, P., SHEN, W., Milicevic, K., Bogdanović Pristov, J., Audinat, E.,& Nikolic, L.. (2022). Therapeutic Potential of Astrocyte Purinergic Signalling in Epilepsy and Multiple Sclerosis. in Frontiers in Pharmacology
Frontiers Media., 13, 900337.
https://doi.org/10.3389/fphar.2022.900337

Nobili P, SHEN W, Milicevic K, Bogdanović Pristov J, Audinat E, Nikolic L. Therapeutic Potential of Astrocyte Purinergic Signalling in Epilepsy and Multiple Sclerosis. in Frontiers in Pharmacology. 2022;13:900337.
doi:10.3389/fphar.2022.900337 .

Nobili, Paola, SHEN, Weida, Milicevic, Katarina, Bogdanović Pristov, Jelena, Audinat, Etienne, Nikolic, Ljiljana, "Therapeutic Potential of Astrocyte Purinergic Signalling in Epilepsy and Multiple Sclerosis" in Frontiers in Pharmacology, 13 (2022):900337,
https://doi.org/10.3389/fphar.2022.900337 . .