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Excitotoxicity

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https://www.readbyqxmd.com/read/29675578/the-parkinson-s-disease-linked-protein-dj-1-associates-with-cytoplasmic-mrnp-granules-during-stress-and-neurodegeneration
#1
Mariaelena Repici, Mahdieh Hassanjani, Daniel C Maddison, Pedro Garção, Sara Cimini, Bhavini Patel, Éva M Szegö, Kornelis R Straatman, Kathryn S Lilley, Tiziana Borsello, Tiago F Outeiro, Lia Panman, Flaviano Giorgini
Mutations in the gene encoding DJ-1 are associated with autosomal recessive forms of Parkinson's disease (PD). DJ-1 plays a role in protection from oxidative stress, but how it functions as an "upstream" oxidative stress sensor and whether this relates to PD is still unclear. Intriguingly, DJ-1 may act as an RNA binding protein associating with specific mRNA transcripts in the human brain. Moreover, we previously reported that the yeast DJ-1 homolog Hsp31 localizes to stress granules (SGs) after glucose starvation, suggesting a role for DJ-1 in RNA dynamics...
April 19, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29674253/involvement-of-snare-complex-in-the-hippocampus-and-prefrontal-cortex-of-offspring-with-depression-induced-by-prenatal-stress
#2
Yan Jun Cao, Qiong Wang, Xing Xing Zheng, Ying Cheng, Yan Zhang
BACKGROUND: Prenatal stress (PS) exposure can cause depression-like behavior in offspring, and maladaptive responses including physiological and neurobiological changes. Glutamate neurotransmission is implicated in effects of PS and in antidepressant mechanisms; however, the mechanisms underlying its involvement remain unclear. In the synapse, the formation of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex is essential for vesicular docking and neurotransmitter release...
April 6, 2018: Journal of Affective Disorders
https://www.readbyqxmd.com/read/29670611/advances-in-biomarker-guided-therapy-for-pediatric-and-adult-onset-neuroinflammatory-disorders-targeting-chemokines-cytokines
#3
REVIEW
Michael R Pranzatelli
The concept and recognized components of "neuroinflammation" are expanding at the intersection of neurobiology and immunobiology. Chemokines (CKs), no longer merely necessary for immune cell trafficking and positioning, have multiple physiologic, developmental, and modulatory functionalities in the central nervous system (CNS) through neuron-glia interactions and other mechanisms affecting neurotransmission. They issue the "help me" cry of neurons and astrocytes in response to CNS injury, engaging invading lymphoid cells (T cells and B cells) and myeloid cells (dendritic cells, monocytes, and neutrophils) (adaptive immunity), as well as microglia and macrophages (innate immunity), in a cascade of events, some beneficial (reparative), others destructive (excitotoxic)...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29668855/the-negative-ultraslow-potential-electrophysiological-correlate-of-infarction-in-the-human-cortex
#4
Janos Lückl, Coline L Lemale, Vasilis Kola, Viktor Horst, Uldus Khojasteh, Ana I Oliveira-Ferreira, Sebastian Major, Maren K L Winkler, Eun-Jeung Kang, Karl Schoknecht, Peter Martus, Jed A Hartings, Johannes Woitzik, Jens P Dreier
Spreading depolarizations are characterized by abrupt, near-complete breakdown of the transmembrane ion gradients, neuronal oedema, mitochondrial depolarization, glutamate excitotoxicity and activity loss (depression). Spreading depolarization induces either transient hyperperfusion in normal tissue; or hypoperfusion (inverse coupling = spreading ischaemia) in tissue at risk for progressive injury. The concept of the spreading depolarization continuum is critical since many spreading depolarizations have intermediate characteristics, as opposed to the two extremes of spreading depolarization in either severely ischaemic or normal tissue...
April 16, 2018: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29666570/role-of-caspase-8-and-fas-in-cell-death-after-spinal-cord-injury
#5
REVIEW
Daniel Sobrido-Cameán, Antón Barreiro-Iglesias
Spinal cord injury (SCI) causes the death of neurons and glial cells due to the initial mechanical forces (i.e., primary injury) and through a cascade of secondary molecular events (e.g., inflammation or excitotoxicity) that exacerbate cell death. The loss of neurons and glial cells that are not replaced after the injury is one of the main causes of disability after SCI. Evidence accumulated in last decades has shown that the activation of apoptotic mechanisms is one of the factors causing the death of intrinsic spinal cord (SC) cells following SCI...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29660340/alteration-of-global-protein-sumoylation-in-neurons-and-astrocytes-in-response-to-alzheimer-s-disease-associated-insults
#6
Takuma Maruyama, Harmony Wada, Yoichiro Abe, Takako Niikura
SUMOylation, a post-translational modification of lysine residues by small ubiquitin-like modifier (SUMO) proteins, has been implicated in the pathogenesis of neurodegenerative disorders including Alzheimer's disease (AD), and in neuron- and astrocyte-specific physiological functions. Global SUMOylation is increased in the AD mouse brain in the pre-plaque-forming stage but returns to wild-type levels in the plaque-bearing stage. To clarify the reason for the transient change in SUMOylation, we analyzed the alteration of global SUMOylation induced by AD-associated cytotoxic stimuli in neurons and astrocytes individually...
April 13, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29659357/-post-stroke-epilepsy
#7
Federico Rodríguez Lucci, Matías Alet, Sebastián F Ameriso
Stroke is the most common cause of seizures and epilepsy in population stuies of adults. Seizures occur within 24 hours of the stroke in a high percent of patients. The pathogenesis of these early-onset seizures may be related to local ion shifts and release of high levels of excitotoxic neurotransmitters in the area of ischemic injury. The risk of late-onset seizures may increase over time, an underlying permanent lesion that leads to persistent chnges in neuronal excitability appears to be responsible for late-onset seizures after stroke...
2018: Medicina
https://www.readbyqxmd.com/read/29658368/the-aaa-atpase-thorase-is-neuroprotective-against-ischemic-injury
#8
Jianmin Zhang, Jia Yang, Huaishan Wang, Omar Sherbini, Matthew J Keuss, George Ke Umanah, Emily Ling-Lin Pai, Zhikai Chi, Kaisa Ma Paldanius, Wei He, Hong Wang, Shaida A Andrabi, Ted M Dawson, Valina L Dawson
Neuronal preconditioning in vitro or in vivo with a stressful but non-lethal stimulus leads to new protein expression that mediates a profound neuroprotection against glutamate excitotoxicity and experimental stroke. The proteins that mediate neuroprotection are relatively unknown and under discovery. Here we find that the expression of the AAA + ATPase Thorase is induced by preconditioning stimulation both in vitro and in vivo. Thorase provides neuroprotection in an ATP-dependent manner against oxygen-glucose deprivation (OGD) neurotoxicity or glutamate N-Methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity in vitro...
January 1, 2018: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/29623030/on-the-role-of-store-operated-calcium-entry-in-acute-and-chronic-neurodegenerative-diseases
#9
REVIEW
Agnese Secondo, Giacinto Bagetta, Diana Amantea
In both excitable and non-excitable cells, calcium (Ca2+ ) signals are maintained by a highly integrated process involving store-operated Ca2+ entry (SOCE), namely the opening of plasma membrane (PM) Ca2+ channels following the release of Ca2+ from intracellular stores. Upon depletion of Ca2+ store, the stromal interaction molecule (STIM) senses Ca2+ level reduction and migrates from endoplasmic reticulum (ER)-like sites to the PM where it activates the channel proteins Orai and/or the transient receptor potential channels (TRPC) prompting Ca2+ refilling...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29617444/ambient-but-not-local-lactate-underlies-neuronal-tolerance-to-prolonged-glucose-deprivation
#10
Courtney Sobieski, Natasha Warikoo, Hong-Jin Shu, Steven Mennerick
Neurons require a nearly constant supply of ATP. Glucose is the predominant source of brain ATP, but the direct effects of prolonged glucose deprivation on neuronal viability and function remain unclear. In sparse rat hippocampal microcultures, neurons were surprisingly resilient to 16 h glucose removal in the absence of secondary excitotoxicity. Neuronal survival and synaptic transmission were unaffected by prolonged removal of exogenous glucose. Inhibition of lactate transport decreased microculture neuronal survival during concurrent glucose deprivation, suggesting that endogenously released lactate is important for tolerance to glucose deprivation...
2018: PloS One
https://www.readbyqxmd.com/read/29614843/role-of-plant-derived-flavonoids-and-their-mechanism-in-attenuation-of-alzheimer-s-and-parkinson-s-diseases-an-update-of-recent-data
#11
REVIEW
Ghulam Hussain, Longbin Zhang, Azhar Rasul, Haseeb Anwar, Muhammad Umar Sohail, Aroona Razzaq, Nimra Aziz, Asghar Shabbir, Muhammad Ali, Tao Sun
Neurodegeneration is a progressive loss of neuronal cells in certain regions of the brain. Most of the neurodegenerative disorders (NDDs) share the communal characteristic such as damage or reduction of various cell types typically including astrocytes and microglial activity. Several compounds are being trialed to treat NDDs but they possess solitary symptomatic advantages along with copious side effects. The finding of more enthralling and captivating compounds to suspend and standstill the pathology of NDDs will be considered as a hallmark of present times...
April 2, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/29610157/clinical-benefit-of-nmda-receptor-antagonists-in-a-patient-with-atp1a2-gene-mutation
#12
Keisuke Ueda, Fatema Serajee, Ahm M Huq
Mutations in the ATP1A2 gene cause familial hemiplegic migraine type 2, alternating hemiplegia of childhood, and cerebellar function deficits, epilepsy, and mental retardation. These symptoms are likely related to glutamatergic hyperexcitability. Our patient is a 12-year-old boy with a history of complex partial seizures, attention-deficit/hyperactivity disorder, and fine motor difficulty. During early childhood, he had episodes of a self-resolving right-sided hemiparesis and focal epilepsy. His seizures did not respond to several antiepileptic medications but stopped after he received valproate...
April 2018: Pediatrics
https://www.readbyqxmd.com/read/29608502/xenon-an-emerging-neuroprotectant-with-potential-application-for-cardiac-arrest-care
#13
Mohammad Roostan, William H Frishman
Xenon is an inert, highly polarizable noble gas with demonstrated safety and application in general anesthesia for over fifty years. A potent inhibitor of the N-methyl-D-aspartate subtype of glutamate receptors, xenon has a well-documented ameliorating effect on excitotoxic neuronal injury in numerous cellular and animal models of hypoxic-ischemic brain injury. The most important determinant of overall survival and morbidity in out-of-hospital cardiac arrest is the severity of neurological injury. The only approved neuroprotective strategy in this setting is mild therapeutic hypothermia, which has demonstrated significant, albeit modest, improvements in mortality...
March 30, 2018: Cardiology in Review
https://www.readbyqxmd.com/read/29607941/gyy4137-an-extended-release-hydrogen-sulfide-donor-reduces-nmda-induced-neuronal-injury-in-the-murine-retina
#14
Kohei Sone, Asami Mori, Kenji Sakamoto, Tsutomu Nakahara
We previously reported that systemic administration with sodium hydrogen sulfide, a rapid-release donor compound of hydrogen sulfide (H2 S), protected retinal neurons against N-methyl-D-aspartic acid (NMDA)-induced injury. For clinical application of H2 S donors for retinal neurodegeneration, topical administration with an extended-release donor compound will be better. In the present study, we histologically investigated whether GYY4137, an extended-release hydrogen sulfide donor, had a protective effect on NMDA-induced retinal injury in the mice in vivo...
2018: Biological & Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/29590100/glial-loss-of-the-metallo-%C3%AE-lactamase-domain-containing-protein-swip-10-induces-age-and-glutamate-signaling-dependent-dopamine-neuron-degeneration
#15
Chelsea L Gibson, Joseph T Balbona, Ashlin Niedzwiecki, Peter Rodriguez, Ken C Q Nguyen, David H Hall, Randy D Blakely
Across phylogeny, glutamate (Glu) signaling plays a critical role in regulating neural excitability, thus supporting many complex behaviors. Perturbed synaptic and extrasynaptic Glu homeostasis in the human brain has been implicated in multiple neuropsychiatric and neurodegenerative disorders including Parkinson's disease, where theories suggest that excitotoxic insults may accelerate a naturally occurring process of dopamine (DA) neuron degeneration. In C. elegans, mutation of the glial expressed gene, swip-10, results in Glu-dependent DA neuron hyperexcitation that leads to elevated DA release, triggering DA signaling-dependent motor paralysis...
March 28, 2018: PLoS Genetics
https://www.readbyqxmd.com/read/29588126/effects-of-12-month-double-blind-n-acetyl-cysteine-on-symptoms-cognition-and-brain-morphology-in-early-phase-schizophrenia-spectrum-disorders
#16
Alan Breier, Emily Liffick, Tom A Hummer, Jenifer L Vohs, Ziyi Yang, Nicole F Mehdiyoun, Andrew C Visco, Emmalee Metzler, Ying Zhang, Michael M Francis
BACKGROUND: Currently approved medications for schizophrenia are relatively ineffective for negative symptoms and cognitive impairment. N-Acetyl Cysteine (NAC) is a neuroprotective agent that improved general symptoms, cognitive impairment and negative symptoms in some but not all studies, but failed to improve positive symptoms in patients with schizophrenia. Progressive brain mass loss (PBML) has been consistently observed in early phase schizophrenia. NAC mitigates the deleterious effects oxidative stress, inflammation and glutamatergic excitotoxicity and these three pathological processes are hypothesized to contribute to PBML...
March 24, 2018: Schizophrenia Research
https://www.readbyqxmd.com/read/29582256/probiotic-treatment-reduces-the-autistic-like-excitation-inhibition-imbalance-in-juvenile-hamsters-induced-by-orally-administered-propionic-acid-and-clindamycin
#17
Afaf El-Ansary, Abir Ben Bacha, Geir Bjørklund, Nora Al-Orf, Ramesa Shafi Bhat, Nadine Moubayed, Kawther Abed
Increasing evidence suggests that the gut microbiota plays a key role in the central nervous system (CNS), and alterations of the gut microbiota composition due to environmental factors can contribute to neurodevelopmental disorders. Animal modeling may help to identify drugs that can normalize the altered gut microbiota and thereby ameliorate abnormal brain signaling pathways. The purpose of the present study was to investigate the therapeutic potency of probiotics such as Bifidobacteria and Lactobacilli on glutamate excitotoxicity as a neurotoxic effect induced by clindamycin and propionic acid (PPA) in juvenile hamsters...
March 27, 2018: Metabolic Brain Disease
https://www.readbyqxmd.com/read/29577894/bilateral-quinolinic-acid-induced-lipid-peroxidation-decreased-striatal-monoamine-levels-and-neurobehavioral-deficits-are-ameliorated-by-gip-receptor-agonist-d-ala-2-gip-in-rat-model-of-huntington-s-disease
#18
Mahip K Verma, Rajan Goel, Krishnadas Nandakumar, Kumar V S Nemmani
Huntington's disease (HD) is an inherited complex progressive neurodegenerative disorder with an established etiopathology linked to neuronal oxidative stress and corticostriatal excitotoxicity. Present study explores the effects of glucose-dependent insulinotropic polypeptide (GIP) receptor agonist on the neurobehavioral sequelae of quinolinic acid-induced phenotype of Huntington's disease in rats. Bilateral administration of quinolinic acid (300 nmol/4µL) to the rat striatum led to characteristic deficits in, locomotor activity, motor coordination, neuromuscular coordination and short-term episodic memory...
March 22, 2018: European Journal of Pharmacology
https://www.readbyqxmd.com/read/29577585/nnos-capon-interaction-mediates-amyloid-%C3%AE-induced-neurotoxicity-especially-in-the-early-stages
#19
Yu Zhang, Zhu Zhu, Hai-Ying Liang, Lei Zhang, Qi-Gang Zhou, Huan-Yu Ni, Chun-Xia Luo, Dong-Ya Zhu
In neurons, increased protein-protein interactions between neuronal nitric oxide synthase (nNOS) and its carboxy-terminal PDZ ligand (CAPON) contribute to excitotoxicity and abnormal dendritic spine development, both of which are involved in the development of Alzheimer's disease. In models of Alzheimer's disease, increased nNOS-CAPON interaction was detected after treatment with amyloid-β in vitro, and a similar change was found in the hippocampus of APP/PS1 mice (a transgenic mouse model of Alzheimer's disease), compared with age-matched background mice in vivo...
March 25, 2018: Aging Cell
https://www.readbyqxmd.com/read/29572690/human-ischaemic-cascade-studies-using-sh-sy5y-cells-a-systematic-review-and-meta-analysis
#20
Ye Liu, Emma D Eaton, Taryn E Wills, Sarah K McCann, Ana Antonic, David W Howells
Low translational yield for stroke may reflect the focus of discovery science on rodents rather than humans. Just how little is known about human neuronal ischaemic responses is confirmed by systematic review and meta-analysis revealing that data for the most commonly used SH-SY5Y human cells comprises only 84 papers. Oxygen-glucose deprivation, H2 O2 , hypoxia, glucose-deprivation and glutamate excitotoxicity yielded - 58, - 61, - 29, - 45 and - 49% injury, respectively, with a dose-response relationship found only for H2 O2 injury (R2  = 29...
March 23, 2018: Translational Stroke Research
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