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Epileptogenesis

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https://www.readbyqxmd.com/read/28212985/nonsteroidal-anti-inflammatory-drugs-in-clinical-and-experimental-epilepsy
#1
REVIEW
Beatrice Mihaela Radu, Florin Bogdan Epureanu, Mihai Radu, Paolo Francesco Fabene, Giuseppe Bertini
Current antiepileptic drugs have limited efficacy and provide little or no benefits in 30% of the patients. Given that a role for brain inflammation in epilepsy has been repeatedly reported in recent years, the potential of anti-inflammatory drugs should be explored in depth, as they may provide new therapeutical approaches in preventing or reducing epileptogenesis. Here, we review preclinical (both in vivo and in vitro) and clinical epilepsy studies in which nonsteroidal antiinflammatory drugs (NSAIDs), i...
February 9, 2017: Epilepsy Research
https://www.readbyqxmd.com/read/28210849/developmental-changes-in-notch1-and-nle1-expression-in-a-genetic-model-of-absence-epilepsy
#2
Fariba Karimzadeh, Sayed Mostafa Modarres Mousavi, Fatemeh Alipour, Hassan Hosseini Ravandi, Stjepana Kovac, Ali Gorji
Childhood absence epilepsy (CAE) is an epilepsy syndrome with seizures occurring in the early childhood, highlighting that seizures susceptibility in CAE is dependent on brain development. The Notch 1 signalling pathway is important in brain development, yet the role of the Notch1 signalling pathway in CAE remains elusive. We here explored Notch1 and its modulator notchless homologue 1 (NLE1) expression in WAG/Rij and control rats using immunohistochemistry. Functional Notch 1 effects were assessed in WAG/Rij rats in vivo...
February 16, 2017: Brain Structure & Function
https://www.readbyqxmd.com/read/28210205/the-atp-gated-p2x7-receptor-as-a-target-for-the-treatment-of-drug-resistant-epilepsy
#3
REVIEW
Edward Beamer, Wolfgang Fischer, Tobias Engel
Despite the progress made in the development of new antiepileptic drugs (AEDs), the biggest challenges that epilepsy presents to drug development have remained unchanged for the last 80 years: finding a treatment with potential for modifying disease progression and reducing the percentage of patients resistant to all pharmacological interventions. The mechanism of action of the majority of AEDs is based on blocking Na(+) and/or Ca(2+) channels, promotion of GABA or inhibition of glutamate signaling. In order for further progress to be made, however, a fuller picture of epilepsy will need to be considered, including changes to blood-brain barrier permeability, synaptic plasticity, network reorganization, and gliosis...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28197553/the-role-of-sirt1-in-epileptogenesis
#4
Alicia M Hall, Gary P Brennan, Tiffany M Nguyen, Akanksha Singh-Taylor, Hyun-Seung Mun, Mary J Sargious, Tallie Z Baram
The mechanisms by which brain insults lead to subsequent epilepsy remain unclear. Insults, including trauma, stroke, tumors, infections, and long seizures [status epilepticus (SE)], create a neuronal state of increased metabolic demand or decreased energy supply. Neurons express molecules that monitor their metabolic state, including sirtuins (Sirts). Sirtuins deacetylate cytoplasmic proteins and nuclear histones, and their epigenetic modulation of the chromatin governs the expression of many genes, influencing neuronal properties...
January 2017: ENeuro
https://www.readbyqxmd.com/read/28195308/ca-2-permeable-ampa-receptors-associated-with-epileptogenesis-of-hypothalamic-hamartoma
#5
Hiroki Kitaura, Masaki Sonoda, Sayaka Teramoto, Hiroshi Shirozu, Hiroshi Shimizu, Tadashi Kimura, Hiroshi Masuda, Yosuke Ito, Hitoshi Takahashi, Shin Kwak, Shigeki Kameyama, Akiyoshi Kakita
Hypothalamic hamartoma (HH), composed of neurons and glia without apparent cytologic abnormalities, is a rare developmental malformation in humans. Patients with HH often have characteristic medically refractory gelastic seizures, and intrinsic epileptogenesis within the lesions has been speculated. Herein we provide evidence to suggest that in HH neurons, Ca(2+) permeability through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors is aberrantly elevated. In needle biopsy specimens of HH tissue, field potential recordings demonstrated spontaneous epileptiform activities similar to those observed in other etiologically distinct epileptogenic tissues...
February 13, 2017: Epilepsia
https://www.readbyqxmd.com/read/28194612/simultaneous-intracranial-eeg-fmri-shows-inter-modality-correlation-in-time-resolved-connectivity-within-normal-areas-but-not-within-epileptic-regions
#6
Ben Ridley, Jonathan Wirsich, Gaelle Bettus, Roman Rodionov, Teresa Murta, Umair Chaudhary, David Carmichael, Rachel Thornton, Serge Vulliemoz, Andrew McEvoy, Fabrice Wendling, Fabrice Bartolomei, Jean-Philippe Ranjeva, Louis Lemieux, Maxime Guye
For the first time in research in humans, we used simultaneous icEEG-fMRI to examine the link between connectivity in haemodynamic signals during the resting-state (rs) and connectivity derived from electrophysiological activity in terms of the inter-modal connectivity correlation (IMCC). We quantified IMCC in nine patients with drug-resistant epilepsy (i) within brain networks in 'healthy' non-involved cortical zones (NIZ) and (ii) within brain networks involved in generating seizures and interictal spikes (IZ1) or solely spikes (IZ2)...
February 13, 2017: Brain Topography
https://www.readbyqxmd.com/read/28193882/neuronal-hyperexcitability-in-a-mouse-model-of-scn8a-epileptic-encephalopathy
#7
Luis F Lopez-Santiago, Yukun Yuan, Jacy L Wagnon, Jacob M Hull, Chad R Frasier, Heather A O'Malley, Miriam H Meisler, Lori L Isom
Patients with early infantile epileptic encephalopathy (EIEE) experience severe seizures and cognitive impairment and are at increased risk for sudden unexpected death in epilepsy (SUDEP). EIEE13 [Online Mendelian Inheritance in Man (OMIM) # 614558] is caused by de novo missense mutations in the voltage-gated sodium channel gene SCN8A Here, we investigated the neuronal phenotype of a mouse model expressing the gain-of-function SCN8A patient mutation, p.Asn1768Asp (Nav1.6-N1768D). Our results revealed regional and neuronal subtype specificity in the effects of the N1768D mutation...
February 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28193459/epileptiform-activity-and-behavioral-arrests-in-mice-overexpressing-the-calcium-channel-subunit-%C3%AE-2%C3%AE-1
#8
Leonardo C Faria, Feng Gu, Isabel Parada, Ben Barres, Z David Luo, David A Prince
: The alpha2delta-1 subunit (α2δ-1) of voltage-gated calcium channels is a receptor for astrocyte-secreted thrombospondins that promote developmental synaptogenesis.Alpha2delta-1 receptors are upregulated in models of injury-induced peripheral pain and epileptogenic neocortical trauma associated with an enhancement of excitatory synaptic connectivity. These results lead to the hypothesis that overexpression of α2δ-1 alone in neocortex of uninjured transgenic (TG) mice might result in increased excitatory connectivity and consequent cortical hyperexcitability and epileptiform activity...
February 10, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28190698/therapeutic-effects-of-cannabinoids-in-animal-models-of-seizures-epilepsy-epileptogenesis-and-epilepsy-related-neuroprotection
#9
REVIEW
Evan C Rosenberg, Pabitra H Patra, Benjamin J Whalley
The isolation and identification of the discrete plant cannabinoids in marijuana revived interest in analyzing historical therapeutic claims made for cannabis in clinical case studies and anecdotes. In particular, sources as old as the 11th and 15th centuries claimed efficacy for crude marijuana extracts in the treatment of convulsive disorders, prompting a particularly active area of preclinical research into the therapeutic potential of plant cannabinoids in epilepsy. Since that time, a large body of literature has accumulated describing the effects of several of the >100 individual plant cannabinoids in preclinical models of seizures, epilepsy, epileptogenesis, and epilepsy-related neuroprotection...
February 9, 2017: Epilepsy & Behavior: E&B
https://www.readbyqxmd.com/read/28179120/novel-therapeutic-approaches-for-disease-modification-of-epileptogenesis-for-curing-epilepsy
#10
REVIEW
Bryan L Clossen, Doodipala Samba Reddy
This article describes the recent advances in epileptogenesis and novel therapeutic approaches for the prevention of epilepsy, with a special emphasis on the pharmacological basis of disease-modification of epileptogenesis for curing epilepsy. Here we assess animal studies and human clinical trials of epilepsy spanning 1982-2016. Epilepsy arises from a number of neuronal factors that trigger epileptogenesis, which is the process by which a brain shifts from a normal physiologic state to an epileptic condition...
February 4, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28177687/curcumin-protects-neuronal-cells-against-status-epilepticus-induced-hippocampal-damage-through-induction-of-autophagy-and-inhibition-of-necroptosis
#11
Jin Wang, Yuan Liu, Xiao-Hui Li, Xiang-Chang Zeng, Jian Li, Jun Zhou, Bo Xiao, Kai Hu
Status epilepticus, the most severe form of epilepsy, is characterized by progressive functional and structural damage in the hippocampus, ultimately leading to the development and clinical appearance of spontaneous, recurrent seizures. Though the pathogenesis underlying epileptogenesis processes remains unclear, a substantial body of evidence has shown that status epilepticus acts as an important initial factor in triggering epileptogenesis. Notably, besides classical cell death mechanisms such as apoptosis and necrosis, two novel regulators of cell fate known as necroptosis and autophagy, are demonstrated to be involved in neuronal damage in various neurodegenerative and neuropsychiatric disorders...
December 9, 2016: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28177664/trimetazidine-potentiates-the-antiepileptic-activity-and-ameliorates-the-metabolic-changes-associated-with-pentylentetrazole-kindling-in-rats-treated-with-valproic-acid
#12
Amina Ahmed Sedky, Osama Mahmod Elserafy, Olfat A Hassan, Hala Salah Abdel Kawy, Amany Hasanin, Mona Hussein Raafat
Oxidative stress is implicated in epileptogenesis as well as in the metabolic changes associated with increased risk of atherosclerotic vascular disease in epilepsy. The present work investigated the impact of the antioxidants trimetazidine (TMZ) on the antiepileptic activity of valproic acid (VAP) and on the metabolic and histological changes in hippocampal, aortic and hepatic tissues associated with epilepsy and/or VPA. Rats were divided into: Non-Pentylentetrazole (PTZ) group; subdivided into: control and VPA treated groups, PTZ-treated group subdivided into: PTZ, PTZ/VPA, PTZ/TMZ, PTZ/VPA+TMZ groups...
January 29, 2017: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28167446/various-modifications-of-the-intrahippocampal-kainate-model-of-mesial-temporal-lobe-epilepsy-in-rats-fail-to-resolve-the-marked-rat-to-mouse-differences-in-type-and-frequency-of-spontaneous-seizures-in-this-model
#13
Rebecca Klee, Claudia Brandt, Kathrin Töllner, Wolfgang Löscher
Temporal lobe epilepsy (TLE) is the most common type of acquired epilepsy in adults. TLE can develop after diverse brain insults, including traumatic brain injury, infections, stroke, or prolonged status epilepticus (SE). Post-SE rodent models of TLE are widely used to understand mechanisms of epileptogenesis and develop treatments for epilepsy prevention. In this respect, the intrahippocampal kainate model of TLE in mice is of interest, because highly frequent spontaneous electrographic seizures develop in the kainate focus, allowing evaluation of both anti-seizure and anti-epileptogenic effects of novel drugs with only short EEG recording periods, which is not possible in any other model of TLE, including the intrahippocampal kainate model in rats...
February 3, 2017: Epilepsy & Behavior: E&B
https://www.readbyqxmd.com/read/28167116/therapeutic-potential-of-an-anti-high-mobility-group-box-1-monoclonal-antibody-in-epilepsy
#14
Junli Zhao, Yi Wang, Cenglin Xu, Keyue Liu, Ying Wang, Liying Chen, Xiaohua Wu, Feng Gao, Yi Guo, Junming Zhu, Shuang Wang, Masahiro Nishibori, Zhong Chen
Brain inflammation is a major factor in epilepsy, and the high mobility group box-1 (HMGB1) protein is known to contribute significantly to the generation of seizures. Here, we investigated the therapeutic potential of an anti-HMGB1 monoclonal antibody (mAb) in epilepsy. Anti-HMGB1 mAb attenuated both acute seizure models (maximal electroshock seizure pentylenetetrazole-induced and kindling-induced), and chronic epilepsy model (kainic acid-induced) in a dose-dependent manner. Meanwhile, the anti-HMGB1 mAb also attenuated seizure activities of human brain slices obtained from surgical resection from drug-resistant epilepsy patients...
February 3, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28166388/toll-like-receptor-3-deficiency-decreases-epileptogenesis-in-a-pilocarpine-model-of-se-induced-epilepsy-in-mice
#15
Adi Gross, Felix Benninger, Ravit Madar, Tomer Illouz, Kathleen Griffioen, Israel Steiner, Daniel Offen, Eitan Okun
OBJECTIVE: Epilepsy affects 60 million people worldwide. Despite the development of antiepileptic drugs, up to 35% of patients are drug refractory with uncontrollable seizures. Toll-like receptors (TLRs) are central components of the nonspecific innate inflammatory response. Because TLR3 was recently implicated in neuronal plasticity, we hypothesized that it may contribute to the development of epilepsy after status epilepticus (SE). METHODS: To test the involvement of TLR3 in epileptogenesis, we used the pilocarpine model for SE in TLR3-deficient mice and their respective wild-type controls...
February 6, 2017: Epilepsia
https://www.readbyqxmd.com/read/28153692/chronic-demyelination-induced-seizures
#16
Andrew S Lapato, Jenny Szu, Jonathan P C Hasselmann, Anna J Khalaj, Devin K Binder, Seema K Tiwari-Woodruff
Multiple sclerosis (MS) patients are three to six times more likely to develop epilepsy compared to the rest of the population. Seizures are more common in patients with early onset or progressive forms of the disease and prognosticate rapid progression to disability and death. Gray matter atrophy, hippocampal lesions, interneuron loss, and elevated juxtacortical lesion burden have been identified in MS patients with seizures; however, translational studies aimed at elucidating the pathophysiological processes underlying MS epileptogenesis are limited...
January 30, 2017: Neuroscience
https://www.readbyqxmd.com/read/28150440/chronic-inhibition-of-brain-glycolysis-initiates-epileptogenesis
#17
Evgeniya Samokhina, Irina Popova, Anton Malkov, Anton I Ivanov, Daniela Papadia, Alexander Osypov, Maxim Molchanov, Svetlana Paskevich, André Fisahn, Misha Zilberter, Yuri Zilberter
Metabolic abnormalities found in epileptogenic tissue provide considerable evidence of brain hypometabolism, while major risk factors for acquired epilepsy all share brain hypometabolism as one common outcome, suggesting that a breakdown of brain energy homeostasis may actually precede epileptogenesis. However, a causal link between deficient brain energy metabolism and epilepsy initiation has not been yet established. To address this issue we developed an in vivo model of chronic energy hypometabolism by daily intracerebroventricular (i...
February 2, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/28149289/pore-forming-proteins-as-mediators-of-novel-epigenetic-mechanism-of-epilepsy
#18
Andrei Surguchov, Irina Surgucheva, Mukut Sharma, Ram Sharma, Vikas Singh
Epilepsy is a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures. In the last two decades, numerous gene defects underlying different forms of epilepsy have been identified with most of these genes encoding ion channel proteins. Despite these developments, the etiology of majority of non-familial epilepsies has no known associated genetic mutations and cannot be explained by defects in identified ion channels alone. We hypothesize that de novo formation of ion channels by naturally unfolded proteins (NUPs) increases neuronal excitability...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28141740/preventing-cognitive-impairment-in-children-with-epilepsy
#19
Kees P J Braun
PURPOSE OF REVIEW: Cognitive impairments are common in children with epilepsy. They may already be present before the onset of epilepsy or occur - and even progress - during its course. Many variables contribute to cognitive dysfunction. Those that can be targeted to prevent (further) cognitive impairment will be highlighted in this review. RECENT FINDINGS: Ideally, but not yet realistically, epileptogenesis is prevented to avert seizures and cognitive impairments in high-risk patients...
January 30, 2017: Current Opinion in Neurology
https://www.readbyqxmd.com/read/28137587/chronic-metformin-treatment-facilitates-seizure-termination
#20
Yong Yang, Binglin Zhu, Fangshuo Zheng, Yun Li, Yanke Zhang, Yida Hu, Xuefeng Wang
The AMP-activated protein kinase (AMPK) is a key energy sensor. Its activator metformin could suppress epileptogenesis in the pentylenetetrazol (PTZ) kindling model. However, the effect of metformin on the acute and chronic seizures has not been studied. We first detected the expression of AMPK in the brain tissue of human and mice with chronic seizures, as well as in mice with acute seizures. Second, using behavioral assay and local filed potentials (LFPs) recording, we investigated the effect of chronic metformin treatment on seizures in a acute seizure model and a chronic seizure model...
January 28, 2017: Biochemical and Biophysical Research Communications
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