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Times Cited: 349
Times Cited: 349
Times Cited
Times Co-cited
Similarity
Oligodendrocyte dysfunction in the pathogenesis of amyotrophic lateral sclerosis.
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Oligodendroglia metabolically support axons and contribute to neurodegeneration.
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Onset and progression in inherited ALS determined by motor neurons and microglia.
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Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis.
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Oligodendrocytes contribute to motor neuron death in ALS via SOD1-dependent mechanism.
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Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity.
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Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6.
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Astrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons.
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Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism.
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Microglia induce motor neuron death via the classical NF-κB pathway in amyotrophic lateral sclerosis.
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10
Cell-autonomous requirement of TDP-43, an ALS/FTD signature protein, for oligodendrocyte survival and myelination.
Jia Wang, Wan Yun Ho, Kenneth Lim, Jia Feng, Greg Tucker-Kellogg, Klaus-Armin Nave, Shuo-Chien Ling. Proc Natl Acad Sci U S A 2018
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The role of oligodendroglial dysfunction in amyotrophic lateral sclerosis.
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Dynamics of oligodendrocyte generation and myelination in the human brain.
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C9orf72 is required for proper macrophage and microglial function in mice.
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Astrocytes from familial and sporadic ALS patients are toxic to motor neurons.
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RIPK1 mediates axonal degeneration by promoting inflammation and necroptosis in ALS.
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Motor neuron intrinsic and extrinsic mechanisms contribute to the pathogenesis of FUS-associated amyotrophic lateral sclerosis.
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8
Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.