Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model - Wikidata - awgldk - TriplyDB

Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

http://www.wikidata.org/entity/Q36718274

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Function Over Form: Modeling Groups of Inherited Neurological Conditions in Zebrafish Glucocerebrosidase 1 deficient Danio rerio mirror key pathological aspects of human Gaucher disease and provide evidence of early microglial activation preceding alpha-synuclein-independent neuronal cell death Growth differentiation factor 6 as a putative risk factor in neuromuscular degeneration INaP selective inhibition reverts precocious inter- and motorneurons hyperexcitability in the Sod1-G93R zebrafish ALS model Aberrant regulation of DNA methylation in amyotrophic lateral sclerosis: a new target of disease mechanisms.Modelling amyotrophic lateral sclerosis: progress and possibilities Zebrafish: A marvel of high-throughput biology for 21(st) century toxicology.The cellular and molecular progression of mitochondrial dysfunction induced by 2,4-dinitrophenol in developing zebrafish embryos Wnt Signaling Alteration in the Spinal Cord of Amyotrophic Lateral Sclerosis Transgenic Mice: Special Focus on Frizzled-5 Cellular Expression Pattern Augmented quantal release of acetylcholine at the vertebrate neuromuscular junction following tdp-43 depletion.Neuregulin 1 confers neuroprotection in SOD1-linked amyotrophic lateral sclerosis mice via restoration of C-boutons of spinal motor neurons.Mutant SOD1 protein increases Nav1.3 channel excitability ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling.Altered cortical beta-band oscillations reflect motor system degeneration in amyotrophic lateral sclerosis.Fishing for causes and cures of motor neuron disorders.Loss and gain of FUS function impair neuromuscular synaptic transmission in a genetic model of ALS.Inhibitory dysfunction in amyotrophic lateral sclerosis: future therapeutic opportunities.Impairments in Motor Neurons, Interneurons and Astrocytes Contribute to Hyperexcitability in ALS: Underlying Mechanisms and Paths to Therapy.Zebrafish models in neuropsychopharmacology and CNS drug discovery.NO-sGC Pathway Modulates Ca2+ Release and Muscle Contraction in Zebrafish Skeletal Muscle.ZNStress: a high-throughput drug screening protocol for identification of compounds modulating neuronal stress in the transgenic mutant sod1G93R zebrafish model of amyotrophic lateral sclerosis An open-source method to analyze optokinetic reflex responses in larval zebrafish.A zebrafish model exemplifies the long preclinical period of motor neuron disease.Sqstm1 knock-down causes a locomotor phenotype ameliorated by rapamycin in a zebrafish model of ALS/FTLD.Concise Review: The Cellular Conspiracy of Amyotrophic Lateral Sclerosis.Hyperexcitability in synaptic and firing activities of spinal motoneurons in an adult mouse model of amyotrophic lateral sclerosis.Spontaneous brain activity in the sensorimotor cortex in amyotrophic lateral sclerosis can be negatively regulated by corticospinal fiber integrity.Protein Misfolding in Prion and Prion-Like Diseases: Reconsidering a Required Role for Protein Loss-of-Function.

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Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

http://www.wikidata.org/entity/Q36718274

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2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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name

Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

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Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

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Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

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Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

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Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

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Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

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Annals of Neurology

P1476

Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model

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P2093

Alexander McGown

http://www.w3.org/2001/XMLSchema#string

Alison N Lyon

http://www.w3.org/2001/XMLSchema#string

Christine E Beattie

http://www.w3.org/2001/XMLSchema#string

Huaxia Tong

http://www.w3.org/2001/XMLSchema#string

Jonathan R McDearmid

http://www.w3.org/2001/XMLSchema#string

Natasha Redhead

http://www.w3.org/2001/XMLSchema#string

Niki Panagiotaki

http://www.w3.org/2001/XMLSchema#string

Sufana Al Mashhadi

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Tennore M Ramesh

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P2860

Circuits controlling vertebrate locomotion: moving in a new direction

Pathogenic protein seeding in Alzheimer disease and other neurodegenerative disorders

Inhibitory synaptic regulation of motoneurons: a new target of disease mechanisms in amyotrophic lateral sclerosis.

Automatic and quantitative measurement of protein-protein colocalization in live cells.

A genetic model of amyotrophic lateral sclerosis in zebrafish displays phenotypic hallmarks of motoneuron disease

Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS.

A topographic map of recruitment in spinal cord.

Nerve terminal degeneration is independent of muscle fiber genotype in SOD1 mice

Motor network degeneration in amyotrophic lateral sclerosis: a structural and functional connectivity study.

Skeletal muscle-restricted expression of human SOD1 causes motor neuron degeneration in transgenic mice

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246-258

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scholarly article

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10.1002/ANA.23780

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2

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73

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2012-12-31T00:00:00Z

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234029059

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23281025

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P921

amyotrophic lateral sclerosis

P932

3608830

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