The neural substrates of rapid-onset Dystonia-Parkinsonism. - Wikidata - wikimedia - TriplyDB

The neural substrates of rapid-onset Dystonia-Parkinsonism.

The neural substrates of rapid-onset Dystonia-Parkinsonism.

http://www.wikidata.org/entity/Q24609728

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The sodium-potassium pump is an information processing element in brain computation Intracellular calcium dynamics permit a Purkinje neuron model to perform toggle and gain computations upon its inputs Insights into the Pathology of the α3 Na(+)/K(+)-ATPase Ion Pump in Neurological Disorders; Lessons from Animal Models The thalamostriatal system in normal and diseased states Cerebellar networks with the cerebral cortex and basal ganglia A rat model of hemidystonia induced by 3-nitropropionic acid Alternating hemiplegia of childhood-related neural and behavioural phenotypes in Na+,K+-ATPase α3 missense mutant mice.Striatal cholinergic dysfunction as a unifying theme in the pathophysiology of dystonia The potential roles of T-type Ca2+ channels in motor coordination.Alterations in cerebellar physiology are associated with a stiff-legged gait in Atcay(ji-hes) mice TorsinA hypofunction causes abnormal twisting movements and sensorimotor circuit neurodegeneration The anatomical basis of dystonia: current view using neuroimaging.Tor1a+/- mice develop dystonia-like movements via a striatal dopaminergic dysregulation triggered by peripheral nerve injury.Genetic silencing of olivocerebellar synapses causes dystonia-like behaviour in mice Hypothermia-induced dystonia and abnormal cerebellar activity in a mouse model with a single disease-mutation in the sodium-potassium pump.Cerebellar zonal patterning relies on Purkinje cell neurotransmission.Abnormal nuclear envelope in the cerebellar Purkinje cells and impaired motor learning in DYT11 myoclonus-dystonia mouse models Abnormal high-frequency burst firing of cerebellar neurons in rapid-onset dystonia-parkinsonism.Physiologic changes associated with cerebellar dystonia.Consensus Paper: Towards a Systems-Level View of Cerebellar Function: the Interplay Between Cerebellum, Basal Ganglia, and Cortex Distinct neurological disorders with ATP1A3 mutations Short latency cerebellar modulation of the basal ganglia Altered spontaneous brain activity in patients with hemifacial spasm: a resting-state functional MRI study Deep brain stimulation for movement and other neurologic disorders Deep-Brain Stimulation for Basal Ganglia Disorders.Spotlight on movement disorders: What optogenetics has to offer.Improved motor performance in Dyt1 ΔGAG heterozygous knock-in mice by cerebellar Purkinje-cell specific Dyt1 conditional knocking-out Alternative approaches to modeling hereditary dystonias.Disruption of Purkinje cell function prior to huntingtin accumulation and cell loss in an animal model of Huntington disease.α-synuclein assemblies sequester neuronal α3-Na+/K+-ATPase and impair Na+ gradient A case of rapid-onset dystonia-parkinsonism accompanied by pyramidal tract impairment.Aberrant Purkinje cell activity is the cause of dystonia in a shRNA-based mouse model of Rapid Onset Dystonia-Parkinsonism.Dysfunctions of the basal ganglia-cerebellar-thalamo-cortical system produce motor tics in Tourette syndrome.Convergent mechanisms in etiologically-diverse dystonias Limited regional cerebellar dysfunction induces focal dystonia in mice.Recent advances in the molecular pathogenesis of dystonia-plus syndromes and heredodegenerative dystonias.Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?Na+/K+ ATPase α1 and α3 isoforms are differentially expressed in α- and γ-motoneurons Animal models for dystonia.The focal dystonias: current views and challenges for future research

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The neural substrates of rapid-onset Dystonia-Parkinsonism.

http://www.wikidata.org/entity/Q24609728

description

2011 nî lūn-bûn

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2011 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2011 թվականի փետրվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

The neural substrates of rapid-onset Dystonia-Parkinsonism

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The neural substrates of rapid-onset Dystonia-Parkinsonism.

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The neural substrates of rapid-onset Dystonia-Parkinsonism.

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type

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The neural substrates of rapid-onset Dystonia-Parkinsonism

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The neural substrates of rapid-onset Dystonia-Parkinsonism.

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The neural substrates of rapid-onset Dystonia-Parkinsonism.

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The neural substrates of rapid-onset Dystonia-Parkinsonism

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The neural substrates of rapid-onset Dystonia-Parkinsonism.

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The neural substrates of rapid-onset Dystonia-Parkinsonism.

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Nature Neuroscience

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The neural substrates of rapid-onset Dystonia-Parkinsonism.

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P2093

D Paola Calderon

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

Franca Kraenzlin

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

Kamran Khodakhah

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Rachel Fremont

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P2860

Parkinson's disease: clinical features and diagnosis

Mutations in the Na+/K+ -ATPase alpha3 gene ATP1A3 are associated with rapid-onset dystonia parkinsonism

Mutation I810N in the alpha3 isoform of Na+,K+-ATPase causes impairments in the sodium pump and hyperexcitability in the CNS.

The basal ganglia and cerebellum interact in the expression of dystonic movement

A specific clinical pattern of camptocormia in Parkinson's disease

Dopamine-independent locomotor actions of amphetamines in a novel acute mouse model of Parkinson disease.

The wide spectrum of spinocerebellar ataxias (SCAs)

The phenotypic spectrum of rapid-onset dystonia-parkinsonism (RDP) and mutations in the ATP1A3 gene

Deficiency in Na,K-ATPase alpha isoform genes alters spatial learning, motor activity, and anxiety in mice

Tottering mouse motor dysfunction is abolished on the Purkinje cell degeneration (pcd) mutant background

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805402

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10.1038/NN.2753

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3

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14

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49813929

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1037096573

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21297628

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Parkinson's disease

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3430603

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