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Neuroinflammation and epilepsy

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https://www.readbyqxmd.com/read/29439117/the-pericyte-glia-interface-at-the-blood-brain-barrier
#1
REVIEW
Patrizia Giannoni, Jerome Badaut, Cyril Dargazanli, Alexis Fayd'Herbe De Maudave, Wendy Klement, Vincent Costalat, Nicola Marchi
The cerebrovasculature is a multicellular structure with varying rheological and permeability properties. The outer wall of the brain capillary endothelium is enclosed by pericytes and astrocyte end feet, anatomically assembled to guarantee barrier functions. We, here, focus on the pericyte modifications occurring in disease conditions, reviewing evidence supporting the interplay amongst pericytes, the endothelium, and glial cells in health and pathology. Deconstruction and reactivity of pericytes and glial cells around the capillary endothelium occur in response to traumatic brain injury, epilepsy, and neurodegenerative disorders, impacting vascular permeability and participating in neuroinflammation...
February 14, 2018: Clinical Science (1979-)
https://www.readbyqxmd.com/read/29372545/prospects-of-cannabidiol-for-easing-status-epilepticus-induced-epileptogenesis-and-related-comorbidities
#2
REVIEW
Dinesh Upadhya, Olagide W Castro, Raghavendra Upadhya, Ashok K Shetty
The hippocampus is one of the most susceptible regions in the brain to be distraught with status epilepticus (SE) induced injury. SE can occur from numerous causes and is more frequent in children and the elderly population. Administration of a combination of antiepileptic drugs can abolish acute seizures in most instances of SE but cannot prevent the morbidity typically seen in survivors of SE such as cognitive and mood impairments and spontaneous recurrent seizures. This is primarily due to the inefficiency of antiepileptic drugs to modify the evolution of SE-induced initial precipitating injury into a series of epileptogenic changes followed by a state of chronic epilepsy...
January 25, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29364511/-18-f-ge180-positron-emission-tomographic-imaging-indicates-a-potential-double-hit-insult-in-the-intrahippocampal-kainate-mouse-model-of-temporal-lobe-epilepsy
#3
Mirjam Brackhan, Pablo Bascuñana, Tobias L Ross, Frank M Bengel, Jens P Bankstahl, Marion Bankstahl
OBJECTIVE: Accumulating evidence suggests that brain inflammation, elicited by epileptogenic insults, is involved in epilepsy development. Noninvasive nuclear imaging of brain inflammation in animal models of epileptogenesis represents a diagnostic in vivo approach with potential for direct translation into the clinic. Here, we investigated up-regulation of the translocator protein (TSPO) indicative of microglial activation by serial [18 F]GE180 positron emission tomographic (PET) imaging in a mouse model of temporal lobe epilepsy...
January 24, 2018: Epilepsia
https://www.readbyqxmd.com/read/29356691/the-epileptic-encephalopathy-jungle-from-dr-west-to-the-concepts-of-aetiology-related-and-developmental-encephalopathies
#4
Judith Kalser, Judith H Cross
PURPOSE OF REVIEW: We aim to further disentangle the jungle of terminology of epileptic encephalopathy and provide some insights into the current understanding about the aetiology and pathophysiology of this process. We cover also the key features of epilepsy syndromes of infancy and childhood which are considered at high risk of developing an epileptic encephalopathy. RECENT FINDINGS: The concept of 'epileptic encephalopathy' has progressively been elaborated by the International League Against Epilepsy according to growing clinical and laboratory evidence...
January 19, 2018: Current Opinion in Neurology
https://www.readbyqxmd.com/read/29346658/potential-for-diet-to-prevent-and-remediate-cognitive-deficits-in-neurological-disorders
#5
Heather M Francis, Richard J Stevenson
The pathophysiology of many neurological disorders involves oxidative stress, neuroinflammation, and mitochondrial dysfunction. There is now substantial evidence that diet can decrease these forms of pathophysiology, and an emerging body of literature relatedly suggests that diet can also prevent or even remediate the cognitive deficits observed in neurological disorders that exhibit such pathology (eg, Alzheimer's disease, multiple sclerosis, age-related cognitive decline, epilepsy). The current review summarizes the emerging evidence in relation to whole diets prominent in the scientific literature-ketogenic, caloric restriction, high polyphenol, and Mediterranean diets-and provides a discussion of the possible underlying neurophysiological mechanisms...
January 15, 2018: Nutrition Reviews
https://www.readbyqxmd.com/read/29329108/cracking-novel-shared-targets-between-epilepsy-and-alzheimer-s-disease-need-of-the-hour
#6
Nitika Garg, Rupa Joshi, Bikash Medhi
Epilepsy and Alzheimer's disease (AD) are interconnected. It is well known that seizures are linked with cognitive impairment, and there are various shared etiologies between epilepsy and AD. The connection between hyperexcitability of neurons and cognitive dysfunction in the progression of AD or epileptogenesis plays a vital role for improving selection of treatment for both diseases. Traditionally, seizures occur less frequently and in later stages of age in patients with AD which in turn implies that neurodegeneration causes seizures...
January 12, 2018: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/29261511/biomechanistic-insights-into-the-roles-of-oxidative-stress-in-generating-complex-neurological-disorders
#7
Mohammad Yusuf, Maria Khan, Majed A Robaian, Riaz A Khan
Neurological diseases like Alzheimer's, epilepsy, Parkinsonism, depression, Huntington's disease, and amyotrophic lateral sclerosis prevailing globally are considered to be deeply influenced by oxidative stress based changes in the biochemical settings of the organs. The excess oxygen concentration triggers the production of reactive oxygen species and even the intrinsic antioxidant enzyme system, i.e., SOD, CAT and GSHPx fails to manage their levels and keep them under desirable limits. This consequently leads to oxidation of protein, lipids, and nucleic acids in the brain resulting in apoptosis, proteopathy, proteasomes and mitochondrion dysfunction, glial cell activation as well as neuroinflammation...
June 27, 2017: Biological Chemistry
https://www.readbyqxmd.com/read/29246095/role-of-neuroinflammation-in-evolution-of-childhood-epilepsy
#8
Sookyong Koh
Until a decade ago, epilepsy research had focused mainly on alterations of neuronal activities and excitability. Such neurocentric emphasis has neglected the role of glia and involvement of inflammation in the pathogenesis of epilepsy. It is becoming clear that immune and inflammatory reactions do occur in the brain despite the brain's lack of conventional lymphatic drainage and graft acceptance and the presence of vascular brain barrier that tightly regulates infiltration of blood monocytes and lymphocytes...
January 2018: Journal of Child Neurology
https://www.readbyqxmd.com/read/29230865/glial-source-of-nitric-oxide-in-epileptogenesis-a-target-for-disease-modification-in-epilepsy
#9
REVIEW
Shaunik Sharma, Sreekanth Puttachary, Thimmasettappa Thippeswamy
Epileptogenesis is the process of developing an epileptic condition and/or its progression once it is established. The molecules that initiate, promote, and propagate remarkable changes in the brain during epileptogenesis are emerging as targets for prevention/treatment of epilepsy. Epileptogenesis is a continuous process that follows immediately after status epilepticus (SE) in animal models of acquired temporal lobe epilepsy (TLE). Both SE and epileptogenesis are potential therapeutic targets for the discovery of anticonvulsants and antiepileptogenic or disease-modifying agents...
December 12, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/29197620/role-of-the-fyn-pkc%C3%AE-signaling-in-se-induced-neuroinflammation-and-epileptogenesis-in-experimental-models-of-temporal-lobe-epilepsy
#10
Shaunik Sharma, Steven Carlson, Sreekanth Puttachary, Souvarish Sarkar, Lucas Showman, Marson Putra, Anumantha G Kanthasamy, Thimmasettappa Thippeswamy
Status epilepticus (SE) induces neuroinflammation and epileptogenesis, but the mechanisms are not yet fully delineated. The Fyn, a non-receptor Src family of tyrosine kinase (SFK), and its immediate downstream target, PKCδ are emerging as potential mediators of neuroinflammation. In order to first determine the role of Fyn kinase signaling in SE, we tested the efficacy of a SFK inhibitor, saracatinib (25mg/kg, oral) in C57BL/6J mouse kainate model of acute seizures. Saracatinib pretreatment dampened SE severity and completely prevented mortality...
November 29, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29186698/effect-of-atorvastatin-on-behavioral-alterations-and-neuroinflammation-during-epileptogenesis
#11
Clarissa Vasconcelos de Oliveira, Jéssica Grigoletto, Julia Marion Canzian, Marta Maria Medeiros Frescura Duarte, Thiago Duarte, Ana Flávia Furian, Mauro Schneider Oliveira
Temporal lobe epilepsy (TLE) is the most frequent and medically refractory type of epilepsy in humans. In addition to seizures, patients with TLE suffer from behavioral alterations and cognitive deficits. Poststatus epilepticus model of TLE induced by pilocarpine in rodents has enhanced the understanding of the processes leading to epilepsy and thus, of potential targets for antiepileptogenic therapies. Clinical and experimental evidence suggests that inflammatory processes in the brain may critically contribute to epileptogenesis...
November 26, 2017: Epilepsy & Behavior: E&B
https://www.readbyqxmd.com/read/29182533/early-gabapentin-treatment-during-the-latency-period-increases-convulsive-threshold-reduces-microglial-activation-and-macrophage-infiltration-in-the-lithium-pilocarpine-model-of-epilepsy
#12
Alicia Rossi, Veronica Murta, Jerónimo Auzmendi, Alberto Javier Ramos
The lithium-pilocarpine model of epilepsy reproduces several features of temporal lobe epilepsy in humans, including the chronological timeline of an initial latency period followed by the development of spontaneous seizures. Epilepsy therapies in humans are implemented, as a rule, after the onset of the spontaneous seizures. We here studied the potential effect on epileptogenesis of starting an early treatment during the latency period, in order to prevent the development of spontaneous seizures. Adult male Wistar rats were treated with 3 mEq/kg LiCl, and 20 h later 30 mg/kg pilocarpine...
November 28, 2017: Pharmaceuticals
https://www.readbyqxmd.com/read/29180982/resveratrol-for-easing-status-epilepticus-induced-brain-injury-inflammation-epileptogenesis-and-cognitive-and-memory-dysfunction-are-we-there-yet
#13
REVIEW
Olagide W Castro, Dinesh Upadhya, Maheedhar Kodali, Ashok K Shetty
Status epilepticus (SE) is a medical emergency exemplified by self-sustaining, unceasing seizures or swiftly recurring seizure events with no recovery between seizures. The early phase after SE event is associated with neurodegeneration, neuroinflammation, and abnormal neurogenesis in the hippocampus though the extent of these changes depends on the severity and duration of seizures. In many instances, over a period, the initial precipitating injury caused by SE leads to temporal lobe epilepsy (TLE), typified by spontaneous recurrent seizures, cognitive, memory and mood impairments associated with chronic inflammation, reduced neurogenesis, abnormal synaptic reorganization, and multiple molecular changes in the hippocampus...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/29153613/brain-expression-of-inflammatory-mediators-in-mesial-temporal-lobe-epilepsy-patients
#14
Bárbara Leal, João Chaves, Cláudia Carvalho, Rui Rangel, Agostinho Santos, Andreia Bettencourt, João Lopes, João Ramalheira, Berta M Silva, António Martins da Silva, Paulo P Costa
Neuroinflammation may be central in epileptogenesis. In this study we analysed inflammatory reaction markers in brain tissue of Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis (MTLE-HS) patients. TLR4, IL-1β and IL-10 gene expression as well as the presence of activated HLA-DR+ microglia was evaluated in 23 patients and 10 cadaveric controls. Inflammation characterized by the presence of HLA-DR(+) microglia and TLR4, IL-1β overexpression was evident in hippocampus and anterior temporal cortex of MTLE-HS patients...
December 15, 2017: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29066951/connexin43-and-pannexin-based-channels-in-neuroinflammation-and-cerebral-neuropathies
#15
REVIEW
Denis Sarrouilhe, Catherine Dejean, Marc Mesnil
Connexins (Cx) are largely represented in the central nervous system (CNS) with 11 Cx isoforms forming intercellular channels. Moreover, in the CNS, Cx43 can form hemichannels (HCs) at non-junctional membrane as does the related channel-forming Pannexin1 (Panx1) and Panx2. Opening of Panx1 channels and Cx43 HCs appears to be involved in inflammation and has been documented in various CNS pathologies. Over recent years, evidence has accumulated supporting a link between inflammation and cerebral neuropathies (migraine, Alzheimer's disease (AD), Parkinson's disease (PD), major depressive disorder, autism spectrum disorder (ASD), epilepsy, schizophrenia, bipolar disorder)...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29049053/treatment-options-for-posttraumatic-epilepsy
#16
Lara L Zimmermann, Ryan M Martin, Fady Girgis
PURPOSE OF REVIEW: Posttraumatic seizures (PTS) and posttraumatic epilepsy (PTE) are common and debilitating consequences of traumatic brain injury (TBI). Early PTS result in secondary brain injury by raising intracranial pressure and worsening cerebral edema and metabolic crisis. PTE is a localization-related epilepsy strongly associated with TBI severity, but risk factors for PTE and epileptogenesis are incompletely understood and are active areas of research. Medical management of PTS in adults and children is reviewed...
December 2017: Current Opinion in Neurology
https://www.readbyqxmd.com/read/29031614/high-mobility-group-box-1-is-a-novel-pathogenic-factor-and-a-mechanistic-biomarker-for-epilepsy
#17
Teresa Ravizza, Gaetano Terrone, Alessia Salamone, Federica Frigerio, Silvia Balosso, Daniel J Antoine, Annamaria Vezzani
Approximately 30% of epilepsy patients experience seizures that are not controlled by the available drugs. Moreover, these drugs provide mainly a symptomatic treatment since they do not interfere with the disease's mechanisms. A mechanistic approach to the discovery of key pathogenic brain modifications causing seizure onset, recurrence and progression is instrumental for designing novel and rationale therapeutic interventions that could modify the disease course or prevent its development. In this regard, increasing evidence shows that neuroinflammation is a pathogenic factor in drug-resistant epilepsies...
October 13, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28950818/inflammation-and-epilepsy-preclinical-findings-and-potential-clinical-translation
#18
Gaetano Terrone, Alessia Salamone, Annamaria Vezzani
BACKGROUND: The lack of treatments which can prevent epilepsy development or improve disease prognosis represents an unmet and urgent clinical need. The development of such drugs requires a deep understanding of the mechanisms underlying disease pathogenesis. In the last decade, preclinical studies in models of acute seizures and of chronic epilepsy highlighted that neuroinflammation arising in brain areas of seizure onset and generalization is a key contributor to neuronal hyper-excitability underlying seizure generation...
September 25, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28942474/svct2-expression-and-function-in-reactive-astrocytes-is-a-common-event-in-different-brain-pathologies
#19
Katterine Salazar, Fernando Martínez, Margarita Pérez-Martín, Manuel Cifuentes, Laura Trigueros, Luciano Ferrada, Francisca Espinoza, Natalia Saldivia, Romina Bertinat, Katherine Forman, María José Oviedo, Antonio J López-Gambero, Christian Bonansco, Ernesto R Bongarzone, Francisco Nualart
Ascorbic acid (AA), the reduced form of vitamin C, acts as a neuroprotector by eliminating free radicals in the brain. Sodium/vitamin C co-transporter isoform 2 (SVCT2) mediates uptake of AA by neurons. It has been reported that SVCT2 mRNA is induced in astrocytes under ischemic damage, suggesting that its expression is enhanced in pathological conditions. However, it remains to be established if SVCT expression is altered in the presence of reactive astrogliosis generated by different brain pathologies. In the present work, we demonstrate that SVCT2 expression is increased in astrocytes present at sites of neuroinflammation induced by intracerebroventricular injection of a GFP-adenovirus or the microbial enzyme, neuraminidase...
September 23, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28856625/inhibition-of-p2x7-receptor-ameliorates-nuclear-factor-kappa-b-mediated-neuroinflammation-induced-by-status-epilepticus-in-rat-hippocampus
#20
Cheng Huang, Xiao-Sa Chi, Rui Li, Xin Hu, Hai-Xia Xu, Jin-Mei Li, Dong Zhou
P2X7 receptor (P2X7R) has been reported participating in neuroinflammation in multiple neurological diseases. We explored the role of P2X7R in a rat status epilepticus (SE) model induced by coriaria lactone (CL) and its association with neuroinflammation. Thirty minutes after intracerebroventricular infusion with P2X7R antagonists Brilliant blue G (BBG), A-438079, A-740003, or agonists 2',3'-O-(4-benzoylbenzoyl)-adenosine 5'-triphosphate (BzATP), SE was induced by intramuscular injection of CL in Sprague-Dawley rats...
October 2017: Journal of Molecular Neuroscience: MN
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