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Brain damage by epilepsy

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https://www.readbyqxmd.com/read/28814872/microrna-expression-profiles-in-chronic-epilepsy-rats-and-neuroprotection-from-seizures-by-targeting-mir-344a
#1
Xixia Liu, Yuhan Liao, Xiuxiu Wang, Donghua Zou, Chun Luo, Chongdong Jian, Yuan Wu
MicroRNA (miRNA) is believed to play a crucial role in the cause and treatment of epilepsy by controlling gene expression. However, it is still unclear how miRNA profiles change after multiple prolonged seizures and aggravation of brain injury in chronic epilepsy (CE). To investigate the role of miRNA in epilepsy, we utilized the CE rat models with pentylenetetrazol (PTZ) and miRNA profiles in the hippocampus. miRNA profiles were characterized using miRNA microarray analysis and were compared with the rats in the sham group, which received 0...
2017: Neuropsychiatric Disease and Treatment
https://www.readbyqxmd.com/read/28795432/subcellular-reorganization-and-altered-phosphorylation-of-the-astrocytic-gap-junction-protein-connexin43-in-human-and-experimental-temporal-lobe-epilepsy
#2
Tushar Deshpande, Tingsong Li, Michel K Herde, Albert Becker, Hartmut Vatter, Martin K Schwarz, Christian Henneberger, Christian Steinhäuser, Peter Bedner
Dysfunctional astrocytes are increasingly recognized as key players in the development and progression of mesial temporal lobe epilepsy (MTLE). One of the dramatic changes astrocytes undergo in MTLE with hippocampal sclerosis (HS) is loss of gap junction coupling. To further elucidate molecular mechanism(s) underlying this alteration, we assessed expression, cellular localization and phosphorylation status of astrocytic gap junction proteins in human and experimental MTLE-HS. In addition to conventional confocal analysis of immunohistochemical staining we employed expansion microscopy, which allowed visualization of blood-brain-barrier (BBB) associated cellular elements at a sub-µm scale...
August 10, 2017: Glia
https://www.readbyqxmd.com/read/28794441/tgf%C3%AE-signaling-is-associated-with-changes-in-inflammatory-gene-expression-and-perineuronal-net-degradation-around-inhibitory-neurons-following-various-neurological-insults
#3
Soo Young Kim, Vladimir V Senatorov, Christapher S Morrissey, Kristina Lippmann, Oscar Vazquez, Dan Z Milikovsky, Feng Gu, Isabel Parada, David A Prince, Albert J Becker, Uwe Heinemann, Alon Friedman, Daniela Kaufer
Brain damage due to stroke or traumatic brain injury (TBI), both leading causes of serious long-term disability, often leads to the development of epilepsy. Patients who develop post-injury epilepsy tend to have poor functional outcomes. Emerging evidence highlights a potential role for blood-brain barrier (BBB) dysfunction in the development of post-injury epilepsy. However, common mechanisms underlying the pathological hyperexcitability are largely unknown. Here, we show that comparative transcriptome analyses predict remodeling of extracellular matrix (ECM) as a common response to different types of injuries...
August 9, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28772144/epileptic-rat-brain-tissue-analyzed-by-2d-correlation-raman-spectroscopy
#4
Julia Sacharz, Aleksandra Wesełucha-Birczyńska, Janina Zięba-Palus, Marian H Lewandowski, Rafał Kowalski, Katarzyna Palus, Łukasz Chrobok, Paulina Moskal, Malwina Birczyńska, Agnieszka Sozańska
Absence epilepsy is the neurological disorder characterized by the pathological spike-and wave discharges present in the electroencephalogram, accompanying a sudden loss of consciousness. Experiments were performed on brain slices obtained from young male WAG/Rij rats (2-3weeks old), so that they were sampled before the appearance of brain-damaging seizures symptoms. Two differing brain areas of the rats' brain tissue were studied: the somatosensory cortex (Sc) and the dorsal lateral geniculate nucleus of the thalamus (DLG)...
July 25, 2017: Spectrochimica Acta. Part A, Molecular and Biomolecular Spectroscopy
https://www.readbyqxmd.com/read/28765170/herpes-simplex-virus-type-1-and-alzheimer-s-disease-possible-mechanisms-and-signposts
#5
REVIEW
Ruth F Itzhaki
Support for the concept that herpes simplex virus type 1 (HSV1), when present in the brains of apolipoprotein E-ε4 carriers, is a major risk for Alzheimer's disease (AD) is increasing steadily, with over 120 publications providing direct or indirect evidence relevant to the hypothesis. No articles have contested the concept, apart from 3 published 13-18 yr ago. This review describes very recent studies on the role of HSV1 but refers also to older studies that provide background for some lesser-known related topics not covered in other recent reviews; these include the relevance of herpes simplex encephalitis and of epilepsy to AD, the action of IFN, and the possible relevance of the different types of DNA damage to AD-in particular, those caused by HSV1-and mechanisms of repair of damage...
August 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28762469/impairment-of-gabaergic-system-contributes-to-epileptogenesis-in-glutaric-acidemia-type-i
#6
Mayara Vendramin Pasquetti, Letícia Meier, Samanta Loureiro, Marcelo Ganzella, Bernardo Junges, Letícia Barbieri Caus, Alexandre Umpierrez Amaral, David M Koeller, Stephen Goodman, Michael Woontner, Diogo Onofre Gomes de Souza, Moacir Wajner, Maria Elisa Calcagnotto
OBJECTIVES: Glutaric acidemia type I (GA-I) is an inherited neurometabolic disorder caused by deficiency of glutaryl-CoA dehydrogenase (GCDH) and characterized by increased levels of glutaric, 3-OH-glutaric, and glutaconic acids in the brain parenchyma. The increment of these organic acids inhibits glutamate decarboxylase (GAD) and consequently lowers the γ-aminobutyric acid (GABA) synthesis. Untreated patients exhibit severe neurologic deficits during development, including epilepsy, especially following an acute encephalopathy outbreak...
August 1, 2017: Epilepsia
https://www.readbyqxmd.com/read/28749594/seizure-activity-per-se-does-not-induce-tissue-damage-markers-in-human-neocortical-focal-epilepsy
#7
Laura Rossini, Rita Garbelli, Vadym Gnatkovsky, Giuseppe Didato, Flavio Villani, Roberto Spreafico, Francesco Deleo, Giorgio Lo Russo, Giovanni Tringali, Francesca Gozzo, Laura Tassi, Marco de Curtis
Objective The contribute of recurring seizures to the progression of epileptogenesis is debated. Seizure-induced brain damage is not conclusively demonstrated both in humans and in animal models of epilepsy. We evaluated the expression of brain injury biomarkers on post-surgical brain tissue obtained from 20 patients with frequent seizures and a long history of drug-resistant focal epilepsy. Methods The expression patterns of specific glial, neuronal and inflammatory molecules was evaluated by immunohistochemistry in the core of type II focal cortical dysplasias (FCD-II), at the FCD boundary (perilesion) and in the adjacent normal-appearing area included in the epileptogenic region...
July 27, 2017: Annals of Neurology
https://www.readbyqxmd.com/read/28685385/exclusive-activation-of-caspase-3-in-mossy-fibers-and-altered-dynamics-of-autophagy-markers-in-the-mice-hippocampus-upon-status-epilepticus-induced-by-kainic-acid
#8
A Rami, A Benz
Epileptic seizures are generally associated with pathological changes in the hippocampus such as astrogliosis, mossy fiber sprouting, and neuronal damage. However, more than 30% of temporal lobe epilepsy in humans shows neither neuronal damage nor mossy fiber sprouting despite chronic epileptic seizures. A similar situation exists in certain commonly used strains of mice, specifically C57BL/6 and BALB/c, which exhibit epileptic seizures, but no neuronal damage upon kainic acid administration. This suggests that intrinsic factors may influence the pathological manifestations of epilepsy...
July 6, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28664455/neuroprotective-effects-of-the-absence-of-jnk1-or-jnk3-isoforms-on-kainic-acid-induced-temporal-lobe-epilepsy-like-symptoms
#9
Luisa de Lemos, Felix Junyent, Antoni Camins, Rubén Darío Castro-Torres, Jaume Folch, Jordi Olloquequi, Carlos Beas-Zarate, Ester Verdaguer, Carme Auladell
The activation of c-Jun-N-terminal kinases (JNK) pathway has been largely associated with the pathogenesis and the neuronal death that occur in neurodegenerative diseases. Altogether, this justifies why JNKs have become a focus of screens for new therapeutic strategies. The aim of the present study was to identify the role of the different JNK isoforms (JNK1, JNK2, and JNK3) in apoptosis and inflammation after induction of brain damage. To address this aim, we induced excitotoxicity in wild-type and JNK knockout mice (jnk1 (-/-) , jnk2 (-/-) , and jnk3 (-/-) ) via an intraperitoneal injection of kainic acid, an agonist of glutamic-kainate-receptors, that induce status epilepticus...
June 29, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28637381/role-of-caspase-3-mediated-apoptosis-in-chronic-caspase-3-cleaved-tau-accumulation-and-blood-brain-barrier-damage-in-the-corpus-callosum-after-traumatic-brain-injury-in-rats
#10
Olena Y Glushakova, Andriy O Glushakov, Cesar V Borlongan, Alex B Valadka, Ronald L Hayes, Alexander V Glushakov
Traumatic brain injury (TBI) may be a significant risk factor for development of neurodegenerative disorders such as chronic traumatic encephalopathy (CTE), post-traumatic epilepsy (PTE), and Alzheimer's (AD) and Parkinson's (PD) diseases. Chronic TBI is associated with several pathological features that are also characteristic of neurodegenerative diseases, including tau pathologies, caspase-3-mediated apoptosis, neuroinflammation, and microvascular alterations. The goal of this study was to evaluate changes following TBI in cleaved-caspase-3 and caspase-3-cleaved tau truncated at Asp421, and their relationships to cellular markers potentially associated with inflammation and blood-brain (BBB) barrier damage...
July 21, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28632329/postictal-hypoperfusion-hypoxia-provides-the-foundation-for-a-unified-theory-of-seizure-induced-brain-abnormalities-and-behavioral-dysfunction
#11
REVIEW
Jordan S Farrell, Roberto Colangeli, Marshal D Wolff, Alexandra K Wall, Thomas J Phillips, Antis George, Paolo Federico, G Campbell Teskey
A recent article by Farrell et al. characterizes the phenomenon, mechanisms, and treatment of a local and severe hypoperfusion/hypoxia event that occurs in brain regions following a focal seizure. Given the well-established role of cerebral ischemia/hypoxia in brain damage and behavioral dysfunction in other clinical settings (e.g., stroke, cerebral vasospasm), we put forward a new theory: postictal hypoperfusion/hypoxia is responsible for the negative consequences associated with seizures. Fortunately, inhibition of two separate molecular targets, cyclooxygenase-2 (COX-2) and l-type calcium channels, can prevent the expression of postictal hypoperfusion/hypoxia...
June 20, 2017: Epilepsia
https://www.readbyqxmd.com/read/28612259/apoptosis-following-cortical-spreading-depression-in-juvenile-rats
#12
Ali Jahanbazi Jahan-Abad, Leila Alizadeh, Sajad Sahab Negah, Parastoo Barati, Maryam Khaleghi Ghadiri, Sven G Meuth, Stjepana Kovac, Ali Gorji
Repetitive cortical spreading depression (CSD) can lead to cell death in immature brain tissue. Caspases are involved in neuronal cell death in several CSD-related neurological disorders, such as stroke and epilepsy. Yet, whether repetitive CSD itself can induce caspase activation in adult or juvenile tissue remains unknown. Inducing repetitive CSD in somatosensory cortices of juvenile and adult rats in vivo, we thus aimed to investigate the effect of repetitive CSD on the expression caspase-3, caspase-8, caspase-9, and caspase-12 in different brain regions using immunohistochemistry and western blotting techniques...
June 13, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28522414/therapeutic-potential-of-agmatine-for-cns-disorders
#13
REVIEW
Vivian B Neis, Priscila B Rosa, Gislaine Olescowicz, Ana Lúcia S Rodrigues
Agmatine is a neuromodulator that regulates multiple neurotransmitters and signaling pathways. Several studies have focused on elucidating the mechanisms underlying the neuroprotective effects of this molecule, which seems to be mediated by a reduction in oxidative damage, neuroinflammation, and proapoptotic signaling. Since these events are implicated in acute and chronic excitotoxicity-related disorders (ischemia, epilepsy, traumatic brain injury, spinal cord injury, neurodegenerative, and psychiatric disorders) as well as in nociception, agmatine has been proposed as a therapeutic strategy for the treatment of central nervous system (CNS) disorders...
September 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28516343/therapeutic-dormancy-to-delay-postsurgical-glioma-recurrence-the-past-present-and-promise-of-focal-hypothermia
#14
REVIEW
Didier Wion
Surgery precedes both radiotherapy and chemotherapy as the first-line therapy for glioma. However, despite multimodal treatment, most glioma patients die from local recurrence in the resection margin. Glioma surgery is inherently lesional, and the response of brain tissue to surgery includes hemostasis, angiogenesis, reactive gliosis and inflammation. Unfortunately, these processes are also associated with tumorigenic side-effects. An increasing amount of evidence indicates that the response to a surgery-related brain injury is hijacked by residual glioma cells and participates in the local regeneration of tumor tissues at the resection margin...
July 2017: Journal of Neuro-oncology
https://www.readbyqxmd.com/read/28495374/metyrapone-prevents-brain-damage-induced-by-status-epilepticus-in-the-rat-lithium-pilocarpine-model
#15
Luis García-García, Ahmed A Shiha, Rubén Fernández de la Rosa, Mercedes Delgado, Ágata Silván, Pablo Bascuñana, Jens P Bankstahl, Francisca Gomez, Miguel A Pozo
The status epilepticus (SE) induced by lithium-pilocarpine is a well characterized rodent model of the human temporal lobe epilepsy (TLE) which is accompanied by severe brain damage. Stress and glucocorticoids markedly contribute to exacerbate neuronal damage induced by seizures but the underlying mechanisms are poorly understood. Herein we sought to investigate whether a single administration of metyrapone (150 mg/kg, i.p.), an 11β-hydroxylase inhibitor, enzyme involved in the peripheral and central synthesis of corticosteroids, had neuroprotective properties in this model...
May 8, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28486943/kb-r7943-reduces-4-aminopyridine-induced-epileptiform-activity-in-adult-rats-after-neuronal-damage-induced-by-neonatal-monosodium-glutamate-treatment
#16
Mariana Hernandez-Ojeda, Monica E Ureña-Guerrero, Paola E Gutierrez-Barajas, Jazmin A Cardenas-Castillo, Antoni Camins, Carlos Beas-Zarate
BACKGROUND: Neonatal monosodium glutamate (MSG) treatment triggers excitotoxicity and induces a degenerative process that affects several brain regions in a way that could lead to epileptogenesis. Na(+)/Ca(2+) exchangers (NCX1-3) are implicated in Ca(2+) brain homeostasis; normally, they extrude Ca(2+) to control cell inflammation, but after damage and in epilepsy, they introduce Ca(2+) by acting in the reverse mode, amplifying the damage. Changes in NCX3 expression in the hippocampus have been reported immediately after neonatal MSG treatment...
May 9, 2017: Journal of Biomedical Science
https://www.readbyqxmd.com/read/28482744/accelerated-long-term-forgetting-is-not-epilepsy-specific-evidence-from-childhood-traumatic-brain-injury
#17
Suncica Lah, Carly Black, Michael B Gascoigne, Chloe Gott, Adrienne Epps, Louise Parry
Accelerated long-term forgetting (ALF) is characterized by adequate recall after short, but not long delays. ALF is not detected by standardized neuropsychological memory tests. Currently, the prevailing conceptualization of ALF is of a temporal lobe seizure-related phenomenon. Nevertheless, Mayes and colleagues (2003) proposed that ALF may occur when any of the components of the brain network involved in long-term memory formation, or their interaction, is disrupted. This disruption does not have to be caused by temporal lobe seizures for ALF to occur...
August 11, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28467996/increased-risk-of-bullous-pemphigoid-after-first-ever-stroke-a-population-based-study
#18
Ai-Ling Shen, Hsiu-Li Lin, Hsiu-Chen Lin, Yuan-Fu Tseng, Chien-Yeh Hsu, Che-Yi Chou
BACKGROUND: We hypothesize that autoantibodies are induced after the blood-brain barrier is damaged by stroke and the risk of bullous pemphigoid (BP) is increased after stroke. We assess the risk of BP after first-ever stroke in a nationwide population-based cohort of first-ever stroke patients. METHODS: We extracted data from the Longitudinal Health Insurance Database 2005 and identified patients with first-ever stroke as well as control patients matched for age, gender, and year of enrollment...
2017: Neuro-degenerative Diseases
https://www.readbyqxmd.com/read/28446773/therapeutic-effects-of-anti-hmgb1-monoclonal-antibody-on-pilocarpine-induced-status-epilepticus-in-mice
#19
Li Fu, Keyue Liu, Hidenori Wake, Kiyoshi Teshigawara, Tadashi Yoshino, Hideo Takahashi, Shuji Mori, Masahiro Nishibori
Inflammatory processes in brain tissue have been described in human epilepsy of various etiologies and in experimental models of seizures. High mobility group box-1 (HMGB1) is now recognized as representative of damage-associated molecular patterns (DAMPs). In the present study, we focused on whether anti-HMGB1 antibody treatment could relieve status epilepticus- triggered BBB breakdown and inflammation response in addition to the seizure behavior itself. Pilocarpine and methyl-scopolamine were used to establish the acute seizure model...
April 26, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28446201/anticonvulsant-effects-of-antiaris-toxicaria-aqueous-extract-investigation-using-animal-models-of-temporal-lobe-epilepsy
#20
Priscilla Kolibea Mante, Donatus Wewura Adongo, Eric Woode
BACKGROUND: Antiaris toxicaria has previously shown anticonvulsant activity in acute animal models of epilepsy. The aqueous extract (AAE) was further investigated for activity in kindling with pentylenetetrazole and administration of pilocarpine and kainic acid which mimic temporal lobe epilepsy in various animal species. RESULTS: ICR mice and Sprague-Dawley rats were pre-treated with AAE (200-800 mg kg(-1)) and convulsive episodes induced using pentylenetetrazole, pilocarpine and kainic acid...
April 26, 2017: BMC Research Notes
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