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Excitotoxicity

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https://www.readbyqxmd.com/read/29458024/spinal-cord-specific-deletion-of-the-glutamate-transporter-glt1-causes-motor-neuron-death-in-mice
#1
Kaori Sugiyama, Kohichi Tanaka
Amyotrophic lateral sclerosis (ALS) is a chronic neurodegenerative disorder characterized by the selective loss of motor neurons. The precise mechanisms that cause the selective death of motor neurons remain unclear, but a growing body of evidence suggests that glutamate-mediated excitotoxicity has been considered to play an important role in the mechanisms of motor neuron degeneration in ALS. Reductions in glutamate transporter GLT1 have been reported in animal models of ALS and the motor cortex and spinal cord of ALS patients...
February 16, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29453960/synaptic-dysfunction-and-altered-excitability-in-c9orf72-als-ftd
#2
Alexander Starr, Rita Sattler
Amyotrophic lateral sclerosis (ALS) is characterized by a progressive degeneration of upper and lower motor neurons, resulting in fatal paralysis due to denervation of the muscle. Due to genetic, pathological and symptomatic overlap, ALS is now considered a spectrum disease together with frontotemporal dementia (FTD), the second most common cause of dementia in individuals under the age of 65. Interestingly, in both diseases, there is a large prevalence of RNA binding proteins (RBPs) that are mutated and considered disease-causing, or whose dysfunction contribute to disease pathogenesis...
February 14, 2018: Brain Research
https://www.readbyqxmd.com/read/29452613/the-role-of-plasma-membrane-calcium-atpases-pmcas-in-neurodegenerative-disorders
#3
REVIEW
Parvana Hajieva, Marius W Baeken, Bernd Moosmann
Selective degeneration of differentiated neurons in the brain is the unifying feature of neurodegenerative disorders such as Parkinson's disease (PD) or Alzheimer's disease (AD). A broad spectrum of evidence indicates that initially subtle, but temporally early calcium dysregulation may be central to the selective neuronal vulnerability observed in these slowly progressing, chronic disorders. Moreover, it has long been evident that excitotoxicity and its major toxic effector mechanism, neuronal calcium overload, play a decisive role in the propagation of secondary neuronal death after acute brain injury from trauma or ischemia...
January 10, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29445325/biomarkers-of-amyotrophic-lateral-sclerosis-current-status-and-interest-of-oxysterols-and-phytosterols
#4
REVIEW
Anne Vejux, Amira Namsi, Thomas Nury, Thibault Moreau, Gérard Lizard
Amyotrophic lateral sclerosis (ALS) is a non-demyelinating neurodegenerative disease in adults with motor disorders. Two forms exist: a sporadic form (90% of cases) and a family form due to mutations in more than 20 genes including the Superoxide dismutase 1, TAR DNA Binding Protein, Fused in Sarcoma, chromosome 9 open reading frame 72 and VAPB genes. The mechanisms associated with this pathology are beginning to be known: oxidative stress, glutamate excitotoxicity, protein aggregation, reticulum endoplasmic stress, neuroinflammation, alteration of RNA metabolism...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29444621/excitotoxicity-in-the-pathogenesis-of-neurological-and-psychiatric-disorders-therapeutic-implications
#5
Jordi Olloquequi, Elizabeth Cornejo-Córdova, Ester Verdaguer, Francesc X Soriano, Octavio Binvignat, Carme Auladell, Antoni Camins
Neurological and psychiatric disorders are leading contributors to the global disease burden, having a serious impact on the quality of life of both patients and their relatives. Although the molecular events underlying these heterogeneous diseases remain poorly understood, some studies have raised the idea of common mechanisms involved. In excitotoxicity, there is an excessive activation of glutamate receptors by excitatory amino acids, leading to neuronal damage. Thus, the excessive release of glutamate can lead to a dysregulation of Ca 2+ homeostasis, triggering the production of free radicals and oxidative stress, mitochondrial dysfunction and eventually cell death...
February 1, 2018: Journal of Psychopharmacology
https://www.readbyqxmd.com/read/29441625/biodegradable-spheres-protect-traumatically-injured-spinal-cord-by-alleviating-the-glutamate-induced-excitotoxicity
#6
Dongfei Liu, Jian Chen, Tao Jiang, Wei Li, Yao Huang, Xiyi Lu, Zehua Liu, Weixia Zhang, Zheng Zhou, Qirui Ding, Hélder A Santos, Guoyong Yin, Jin Fan
New treatment strategies for spinal cord injury with good therapeutic efficacy are actively pursued. Here, acetalated dextran (AcDX), a biodegradable polymer obtained by modifying vicinal diols of dextran, is demonstrated to protect the traumatically injured spinal cord. To facilitate its administration, AcDX is formulated into microspheres (≈7.2 µm in diameter) by the droplet microfluidic technique. Intrathecally injected AcDX microspheres effectively reduce the traumatic lesion volume and inflammatory response in the injured spinal cord, protect the spinal cord neurons from apoptosis, and ultimately, recover the locomotor function of injured rats...
February 14, 2018: Advanced Materials
https://www.readbyqxmd.com/read/29435916/the-metabolic-disturbances-of-motoneurons-exposed-to-glutamate
#7
Blandine Madji Hounoum, Hélène Blasco, Emmanuelle Coque, Patrick Vourc'h, Patrick Emond, Philippe Corcia, Christian R Andres, Cédric Raoul, Sylvie Mavel
Glutamate-induced excitotoxicity is considered as one of the major pathophysiological factors of motoneuron death in amyotrophic lateral sclerosis and other motoneuron diseases. In order to expand our knowledge on mechanisms of glutamate-induced excitotoxicity, the present study proposes to determine the metabolic consequences of glutamate and astrocytes in primary enriched motoneuron culture. Using liquid chromatography coupled to high-resolution mass spectrometry (LC-HRMS), we showed that the presence of astrocytes and glutamate profoundly modified the metabolic profile of motoneurons...
February 12, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29430619/a-regulatory-circuitry-between-gria2-mir-409-and-mir-495-is-affected-by-als-fus-mutation-in-esc-derived-motor-neurons
#8
Davide Capauto, Alessio Colantoni, Lei Lu, Tiziana Santini, Giovanna Peruzzi, Silvia Biscarini, Mariangela Morlando, Neil A Shneider, Elisa Caffarelli, Pietro Laneve, Irene Bozzoni
Mutations in fused in sarcoma (FUS) cause amyotrophic lateral sclerosis (ALS). FUS is a multifunctional protein involved in the biogenesis and activity of several types of RNAs, and its role in the pathogenesis of ALS may involve both direct effects of disease-associated mutations through gain- and loss-of-function mechanisms and indirect effects due to the cross talk between different classes of FUS-dependent RNAs. To explore how FUS mutations impinge on motor neuron-specific RNA-based circuitries, we performed transcriptome profiling of small and long RNAs of motor neurons (MNs) derived from mouse embryonic stem cells carrying a FUS-P517L knock-in mutation, which is equivalent to human FUS-P525L, associated with a severe and juvenile-onset form of ALS...
February 12, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29427613/microglial-activation-and-vascular-responses-that-are-associated-with-early-thalamic-neurodegeneration-resulting-from-thiamine-deficiency
#9
John F Bowyer, Karen M Tranter, Sumit Sarkar, Joseph P Hanig
Thiamine/ vitamin B1 deficiency can lead to behavioral changes and neurotoxicity in humans. This may due in part to vascular damage, neuroinflammation and neuronal degeneration in the diencephalon, which is seen in animal models of pyrithiamine-enhanced thiamine deficiency. However, the time course of the progression of these changes in the animal models has been poorly characterized. Therefore, in this study, the progression of: 1) activated microglial association with vasculature; 2) neurodegeneration; and 3) any vascular leakage in the forebrain during the progress of thiamine deficiency were determined...
February 7, 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29427114/pharmacological-therapies-for-machado-joseph-disease
#10
Sara Duarte-Silva, Patrícia Maciel
Machado-Joseph disease (MJD), also known as Spinocerebellar Ataxia type 3 (SCA3), is the most common autosomal dominant ataxia worldwide. MJD integrates a large group of disorders known as polyglutamine diseases (polyQ). To date, no effective treatment exists for MJD and other polyQ diseases. Nevertheless, researchers are making efforts to find treatment possibilities that modify the disease course or alleviate disease symptoms. Since neuroimaging studies in mutation carrying individuals suggest that in nervous system dysfunction begins many years before the onset of any detectable symptoms, the development of therapeutic interventions becomes of great importance, not only to slow progression of manifest disease but also to delay, or ideally prevent, its onset...
2018: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29426351/poly-arginine-r18-and-r18d-d-enantiomer-peptides-reduce-infarct-volume-and-improves-behavioural-outcomes-following-perinatal-hypoxic-ischaemic-encephalopathy-in-the-p7-rat
#11
Adam B Edwards, Jane L Cross, Ryan S Anderton, Neville W Knuckey, Bruno P Meloni
We examined the neuroprotective efficacy of the poly-arginine peptide R18 and its D-enantiomer R18D in a perinatal hypoxic-ischaemic (HI) model in P7 Sprague-Dawley rats. R18 and R18D peptides were administered intraperitoneally at doses of 30, 100, 300 or 1000 nmol/kg immediately after HI (8% O2/92%N2 for 2.5 h). The previously characterised neuroprotective JNKI-1-TATD peptide at a dose of 1000 nmol/kg was used as a control. Infarct volume and behavioural outcomes were measured 48 h after HI. For the R18 and R18D doses examined, total infarct volume was reduced by 25...
February 9, 2018: Molecular Brain
https://www.readbyqxmd.com/read/29425760/agathisflavone-a-flavonoid-derived-from-poincianella-pyramidalis-tul-enhances-neuronal-population-and-protects-against-glutamate-excitotoxicity
#12
Cleide Dos Santos Souza, Maria Socorro Grangeiro, Erica Patricia Lima Pereira, Cleonice Creusa Dos Santos, Alessandra Bispo da Silva, Geraldo Pedral Sampaio, Daiana Dias Ribeiro Figueiredo, Jorge Mauricio David, Juceni Pereira David, Victor Diogenes Amaral da Silva, Arthur Morgan Butt, Silvia Lima Costa
Flavonoids are bioactive compounds that are known to be neuroprotective against glutamate-mediated excitotoxicity, one of the major causes of neurodegeneration. The mechanisms underlying these effects are unresolved, but recent evidence indicates flavonoids may modulate estrogen signaling, which can delay the onset and ameliorate the severity of neurodegenerative disorders. Furthermore, the roles played by glial cells in the neuroprotective effects of flavonoids are poorly understood. The aim of this study was to investigate the effects of the flavonoid agathisflavone (FAB) in primary neuron-glial co-cultures from postnatal rat cerebral cortex...
February 6, 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29425209/retinal-genes-are-differentially-expressed-in-areas-of-primary-versus-secondary-degeneration-following-partial-optic-nerve-injury
#13
Wissam Chiha, Chrisna J LeVaillant, Carole A Bartlett, Alex W Hewitt, Phillip E Melton, Melinda Fitzgerald, Alan R Harvey
BACKGROUND: Partial transection (PT) of the optic nerve is an established experimental model of secondary degeneration in the central nervous system. After a dorsal transection, retinal ganglion cells (RGCs) with axons in ventral optic nerve are intact but vulnerable to secondary degeneration, whereas RGCs in dorsal retina with dorsal axons are affected by primary and secondary injuries. Using microarray, we quantified gene expression changes in dorsal and ventral retina at 1 and 7 days post PT, to characterize pathogenic pathways linked to primary and secondary degeneration...
2018: PloS One
https://www.readbyqxmd.com/read/29417476/qi-fu-yin-a-ming-dynasty-prescription-for-the-treatment-of-dementia
#14
REVIEW
Wei-Yi Ong, Ya-Jun Wu, Tahira Farooqui, Akhlaq A Farooqui
The Traditional Chinese Medicine (TCM) theory that "kidneys give rise to marrow, and the brain is the sea of marrow" has been a guide for the clinical application of kidney, qi and blood tonics for prevention and treatment of dementia and improvement in memory. As low resistance end-organs, both the brain and the kidneys are subjected to blood flow of high volumes throughout the cardiac cycle. Alzheimer's disease and vascular dementia are two common causes of dementia, and it is increasingly recognized that many older adults with dementia have both AD and vascular pathologies...
February 7, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29417050/d-amino-acid-oxidase-plg72-interaction-and-d-serine-modulation
#15
REVIEW
Loredano Pollegioni, Luciano Piubelli, Gianluca Molla, Elena Rosini
pLG72 is a small, primate-specific protein of 153 amino acids. It is the product of the G72 gene, expressed in testis, spinal cord, and brain. The presence of G72 transcript and pLG72 has recurrently been called into question, however G72 mRNA and pLG72 protein levels were higher in blood and brain of patients with schizophrenia than in healthy controls. On the one hand, the SNP rs2391191 corresponding to the R30K substitution in pLG72 was genetically linked to schizophrenia, reduced thickness of the brain cortex in schizophrenia-affected individuals, and altered memory function...
2018: Frontiers in Molecular Biosciences
https://www.readbyqxmd.com/read/29413528/nitric-oxide-signaling-in-neurodegeneration-and-cell-death
#16
Ted M Dawson, Valina L Dawson
In this tribute to Solomon H. Snyder (Sol) we discuss the mechanisms by which nitric oxide (NO) kills neurons. We provide a historical perspective regarding the discovery that glutamate excitotoxicity is mediated by NO. It also contains a discussion of the discovery that neuronal nitric oxide synthase (nNOS) catalytic activity accounts for NADPH diaphorase activity and its localization in the central nervous system. NADPH diaphorase/nNOS neurons are unique in that they are resistant to toxic effects of excess glutamate and that they are resistant to neurodegeneration in a variety of neurodegenerative diseases...
2018: Advances in Pharmacology
https://www.readbyqxmd.com/read/29411931/neuroprotective-mechanisms-of-glucagon-like-peptide-1-based-therapies-in-ischaemic-stroke-a-systematic-review-based-on-pre-clinical-studies
#17
Ida R Marlet, Joakim N E Ölmestig, Tina Vilsbøll, Jørgen Rungby, Christina Kruuse
Glucagon-like peptide-1 (GLP-1)-based therapies, GLP-1 receptor agonists (GLP-1RAs), and dipeptidyl peptidase-4 inhibitors (DPP-4Is) are widely used for the treatment of type 2 diabetes. Increasing evidence suggests that they may provide neuroprotection. The aim of this MiniReview was to systematically evaluate the proposed mechanism of action for GLP-1-based therapies in ischaemic brain damage in animals. We performed a literature search using Medline, Embase and The Cochrane Library. GLP-1-based therapies administered before, during or after experimental stroke in diabetic and non-diabetic animals were evaluated...
February 7, 2018: Basic & Clinical Pharmacology & Toxicology
https://www.readbyqxmd.com/read/29410613/neuronal-lipid-metabolism-multiple-pathways-driving-functional-outcomes-in-health-and-disease
#18
REVIEW
Timothy J Tracey, Frederik J Steyn, Ernst J Wolvetang, Shyuan T Ngo
Lipids are a fundamental class of organic molecules implicated in a wide range of biological processes related to their structural diversity, and based on this can be broadly classified into five categories; fatty acids, triacylglycerols (TAGs), phospholipids, sterol lipids and sphingolipids. Different lipid classes play major roles in neuronal cell populations; they can be used as energy substrates, act as building blocks for cellular structural machinery, serve as bioactive molecules, or a combination of each...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29408814/magnesium-as-a-neuroprotective-agent-a-review-of-its-use-in-the-fetus-term-infant-with-neonatal-encephalopathy-and-the-adult-stroke-patient
#19
Ingran Lingam, Nicola J Robertson
Magnesium is an intracellular cation essential for many en-zymatic processes and cellular functions. Magnesium sulfate acts as an endogenous calcium channel antagonist at neuronal synapses, thought to prevent excessive activation of N-methyl-D-aspartate receptors by excitatory amino acids, such as glutamate, and by downregulation of proinflammatory pathways. Early intervention is essential in the prevention of the secondary phase of neuronal injury. The immature brain is particularly prone to excitotoxicity, and inflammation has been strongly implicated in the pathogenesis of cerebral palsy...
February 7, 2018: Developmental Neuroscience
https://www.readbyqxmd.com/read/29408665/selenium-and-zinc-two-key-players-against-cadmium-induced-neuronal-toxicity
#20
Jacopo J V Branca, Gabriele Morucci, Mario Maresca, Barbara Tenci, Roberta Cascella, Ferdinando Paternostro, Carla Ghelardini, Massimo Gulisano, Lorenzo Di Cesare Mannelli, Alessandra Pacini
Cadmium (Cd), a worldwide occupational pollutant, is an extremely toxic heavy metal, capable of damaging several organs, including the brain. Its toxicity has been related to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. The neurotoxic potential of Cd has been attributed to the changes induced in the brain enzyme network involved in counteracting oxidative stress. On the other hand, it is also known that trace elements, such as zinc (Zn) and selenium (Se), required for optimal brain functions, appears to have beneficial effects on the prevention of Cd intoxication...
January 29, 2018: Toxicology in Vitro: An International Journal Published in Association with BIBRA
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