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Impaired Autophagy and Defective Mitochondrial Function: Converging Paths on the Road to Motor Neuron DegenerationAdducin at the Neuromuscular Junction in Amyotrophic Lateral Sclerosis: Hanging on for Dear LifeThere's Something Wrong with my MAM; the ER-Mitochondria Axis and Neurodegenerative DiseasesEmerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and DiseaseNeuroRDF: semantic integration of highly curated data to prioritize biomarker candidates in Alzheimer's diseaseBioenergetic status modulates motor neuron vulnerability and pathogenesis in a zebrafish model of spinal muscular atrophy.α-Synuclein binds to the ER-mitochondria tethering protein VAPB to disrupt Ca2+ homeostasis and mitochondrial ATP productionGenotype-property patient-phenotype relations suggest that proteome exhaustion can cause amyotrophic lateral sclerosis.Molecular determinants of selective dopaminergic vulnerability in Parkinson's disease: an update.The interplay between metabolic homeostasis and neurodegeneration: insights into the neurometabolic nature of amyotrophic lateral sclerosis.Pathogenesis of amyotrophic lateral sclerosis.Management and therapeutic perspectives in amyotrophic lateral sclerosis.ALS/FTD-associated FUS activates GSK-3β to disrupt the VAPB-PTPIP51 interaction and ER-mitochondria associations.Aberrant association of misfolded SOD1 with Na(+)/K(+)ATPase-α3 impairs its activity and contributes to motor neuron vulnerability in ALS.Modeling cytokine regulatory network dynamics driving neuroinflammation in central nervous system disorders.Current technical approaches to brain energy metabolism.The Src/c-Abl pathway is a potential therapeutic target in amyotrophic lateral sclerosis.Analyzing optical imaging of Ca2+ signals via TIRF microscopy: The limits on resolution due to chemical rates and depth of the channels.Capturing intracellular Ca2+ dynamics in computational models of neurodegenerative diseases.Aberrant Subcellular Dynamics of Sigma-1 Receptor Mutants Underlying Neuromuscular Diseases.Energy metabolism in ALS: an underappreciated opportunity?The vulnerability of spinal motoneurons and soma size plasticity in a mouse model of amyotrophic lateral sclerosis.Endoplasmic reticulum and mitochondria in diseases of motor and sensory neurons: a broken relationship?Hypoexcitability precedes denervation in the large fast-contracting motor units in two unrelated mouse models of ALS.Mitochondrial Chaperones in the Brain: Safeguarding Brain Health and Metabolism?Presynaptic loss of dynamin related protein 1 impairs synaptic vesicle release and recycling at the mouse calyx of heldLocalization of RNAi Machinery to Axonal Branch Points and Growth Cones Is Facilitated by Mitochondria and Is Disrupted in ALS
P2860
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P2860
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
2014年论文
@zh
2014年论文
@zh-cn
name
A computational model of motor neuron degeneration.
@en
type
label
A computational model of motor neuron degeneration.
@en
prefLabel
A computational model of motor neuron degeneration.
@en
P2860
P1433
P1476
A computational model of motor neuron degeneration.
@en
P2093
Gwendal Le Masson
L F Abbott
P2860
P304
P356
10.1016/J.NEURON.2014.07.001
P407
P577
2014-07-31T00:00:00Z