scholarly journals Temporal Lobe Epilepsy: Cell Death and Molecular Targets

10.5772/19835 ◽  
2011 ◽  
Author(s):  
Maria Jose da Silva Fernandes ◽  
Esper Abrao ◽  
Joao Pereira ◽  
Daniele Suzete
Keyword(s):  
Cell Death ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Molecular Targets

scholarly journals Induction of the Nrf2 Pathway by Sulforaphane Is Neuroprotective in a Rat Temporal Lobe Epilepsy Model

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1702
Author(s):  
Sereen Sandouka ◽  
Tawfeeq Shekh-Ahmad
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Antioxidant Capacity ◽  
Temporal Lobe ◽  
Epileptiform Activity ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
The Brain

Epilepsy is a chronic disease of the brain that affects over 65 million people worldwide. Acquired epilepsy is initiated by neurological insults, such as status epilepticus, which can result in the generation of ROS and induction of oxidative stress. Suppressing oxidative stress by upregulation of the transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown to be an effective strategy to increase endogenous antioxidant defences, including in brain diseases, and can ameliorate neuronal damage and seizure occurrence in epilepsy. Here, we aim to test the neuroprotective potential of a naturally occurring Nrf2 activator sulforaphane, in in vitro epileptiform activity model and a temporal lobe epilepsy rat model. Sulforaphane significantly decreased ROS generation during epileptiform activity, restored glutathione levels, and prevented seizure-like activity-induced neuronal cell death. When given to rats after 2 h of kainic acid-induced status epilepticus, sulforaphane significantly increased the expression of Nrf2 and related antioxidant genes, improved oxidative stress markers, and increased the total antioxidant capacity in both the plasma and hippocampus. In addition, sulforaphane significantly decreased status epilepticus-induced neuronal cell death. Our results demonstrate that Nrf2 activation following an insult to the brain exerts a neuroprotective effect by reducing neuronal death, increasing the antioxidant capacity, and thus may also modify epilepsy development.

scholarly journals c-JUN Expression and Apoptotic Cell Death in Kainate-Induced Temporal Lobe Epilepsy

2001 ◽  
Vol 16 (5) ◽  
pp. 649 ◽  
Author(s):  
Min Cheol Lee ◽  
Jin Lee Rho ◽  
Myung Kyu Kim ◽  
Young Jong Woo ◽  
Jae Hyoo Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

scholarly journals Parawixin2 Protects Hippocampal Cells in Experimental Temporal Lobe Epilepsy

Toxins ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 486 ◽  
Author(s):  
José Liberato ◽  
Lívea Godoy ◽  
Alexandra Cunha ◽  
Marcia Mortari ◽  
Rene de Oliveira Beleboni ◽  
...  
Keyword(s):  
Cell Death ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Apoptotic Cell ◽  
Hippocampal Sclerosis ◽  
Anticonvulsant Effect ◽  
Dependent Manner ◽  
Neuroprotective Effects ◽  
Gabaergic Neurotransmission ◽  
Wide Range

Epilepsy is considered as one of the major disabling neuropathologies. Almost one third of adult patients with temporal lobe epilepsy (TLE) do not respond to current antiepileptic drugs (AEDs). Additionally, most AEDs do not have neuroprotective effects against the inherent neurodegenerative process underlying the hippocampal sclerosis on TLE. Dysfunctions in the GABAergic neurotransmission may contribute not only to the onset of epileptic activity but also constitute an important system for therapeutic approaches. Therefore, molecules that enhance GABA inhibitory effects could open novel avenues for the understanding of epileptic plasticity and for drug development. Parawixin2, a compound isolated from Parawixia bistriata spider venom, inhibits both GABA and glycine uptake and has an anticonvulsant effect against a wide range of chemoconvulsants. The neuroprotective potential of Parawixin2 was analyzed in a model of TLE induced by a long-lasting Status Epilepticus (SE), and its efficiency was compared to well-known neuroprotective drugs, such as riluzole and nipecotic acid. Neuroprotection was assessed through histological markers for cell density (Nissl), astrocytic reactivity (GFAP) and cell death labeling (TUNEL), which were performed 24 h and 72 h after SE. Parawixin2 treatment resulted in neuroprotective effects in a dose dependent manner at 24 h and 72 h after SE, as well as reduced reactive astrocytes and apoptotic cell death. Based on these findings, Parawixin2 has a great potential to be used as a tool for neuroscience research and as a probe to the development of novel GABAergic neuroprotective agents.

Neuronal Cell Death in a Rat Model for Mesial Temporal Lobe Epilepsy Is Induced by the Initial Status Epilepticus and Not by Later Repeated Spontaneous Seizures

Epilepsia ◽  
2003 ◽  
Vol 44 (5) ◽  
pp. 647-658 ◽  
Author(s):  
Jan A. Gorter ◽  
Pedro M. Gonçalves Pereira ◽  
Erwin A. Van Vliet ◽  
Eleonora Aronica ◽  
Fernando H. Lopes Da Silva ◽  
...  
Keyword(s):  
Cell Death ◽  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Rat Model ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mesial Temporal Lobe Epilepsy ◽  
Spontaneous Seizures ◽  
Mesial Temporal Lobe

scholarly journals Caspase-3 Cleavage and Nuclear Localization of Caspase-Activated DNase in Human Temporal Lobe Epilepsy

2005 ◽  
Vol 26 (4) ◽  
pp. 583-589 ◽  
Author(s):  
Clara K Schindler ◽  
Erik G Pearson ◽  
Helena P Bonner ◽  
Norman K So ◽  
Roger P Simon ◽  
...  
Keyword(s):  
Cell Death ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Nuclear Localization ◽  
Caspase 3 ◽  
Nuclear Accumulation ◽  
Nuclear Fraction ◽  
Endonuclease G ◽  
Caspase Activated Dnase ◽  
Human Temporal Lobe

Programmed cell death (apoptosis) signaling pathways have been implicated in seizure-induced neuronal death and the pathogenesis of human temporal lobe epilepsy (TLE). End-stage DNA fragmentation during cell death may be mediated by nucleases including caspase-activated DNase (CAD), apoptosis-inducing factor (AIF) and endonuclease G. In the present study, we investigated the subcellular localization of these nucleases in resected hippocampus from TLE patients and autopsy controls. Subcellular fractionation determined levels of CAD were significantly higher in the nuclear fraction of TLE samples compared with controls, and semiquantitative immunohistochemistry revealed cleaved caspase-3 positive cells in TLE sections but not controls. While mitochondrial levels of AIF and endonuclease G were higher in TLE samples than controls, nuclear localization of AIF was limited and restricted to cells that were negative for cleaved caspase-3. Nuclear accumulation of endonuclease G was not found in TLE samples. These data support ongoing caspase-dependent apoptosis signaling in human TLE and suggest that interventions targeting such pathways may have potential as adjunctive neuroprotective therapy in epilepsy.

Theory of mind and social competence in children and adolescents with temporal lobe epilepsy.

2019 ◽  
Vol 33 (7) ◽  
pp. 986-995 ◽  
Author(s):  
Elizabeth Stewart ◽  
Cathy Catroppa ◽  
Linda Gonzalez ◽  
Deepak Gill ◽  
Richard Webster ◽  
...  
Keyword(s):  
Theory Of Mind ◽  
Social Competence ◽  
Temporal Lobe Epilepsy ◽  
Children And Adolescents ◽  
Temporal Lobe
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