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Times Cited: 14
Times Cited: 14
Times Cited
Times Co-cited
Similarity
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Mutations of optineurin in amyotrophic lateral sclerosis.
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Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
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A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.
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Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis.
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Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia.
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Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis.
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Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways.
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Oligodendroglia metabolically support axons and contribute to neurodegeneration.
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Knockout of reactive astrocyte activating factors slows disease progression in an ALS mouse model.
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Degeneration and impaired regeneration of gray matter oligodendrocytes in amyotrophic lateral sclerosis.
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TDP-43 pathology and neuronal loss in amyotrophic lateral sclerosis spinal cord.
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ALS Genetics: Gains, Losses, and Implications for Future Therapies.
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Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis.
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TDP-43 is a component of ubiquitin-positive tau-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
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Divergent roles of ALS-linked proteins FUS/TLS and TDP-43 intersect in processing long pre-mRNAs.
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Exome sequencing reveals VCP mutations as a cause of familial ALS.
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Stages of pTDP-43 pathology in amyotrophic lateral sclerosis.
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Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.
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The basis of clinicopathological heterogeneity in TDP-43 proteinopathy.
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Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis.
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Oligodendrocytes contribute to motor neuron death in ALS via SOD1-dependent mechanism.
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Astrocytes as determinants of disease progression in inherited amyotrophic lateral sclerosis.
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Oligodendrocyte heterogeneity in the mouse juvenile and adult central nervous system.
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Onset and progression in inherited ALS determined by motor neurons and microglia.
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Wild-type nonneuronal cells extend survival of SOD1 mutant motor neurons in ALS mice.
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TDP-43 gains function due to perturbed autoregulation in a Tardbp knock-in mouse model of ALS-FTD.
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Microglia induce motor neuron death via the classical NF-κB pathway in amyotrophic lateral sclerosis.
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Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity.
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Conditional depletion of Fus in oligodendrocytes leads to motor hyperactivity and increased myelin deposition associated with Akt and cholesterol activation.
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Pathological heterogeneity in amyotrophic lateral sclerosis with FUS mutations: two distinct patterns correlating with disease severity and mutation.
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Astrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons.
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Human embryonic stem cell-derived motor neurons are sensitive to the toxic effect of glial cells carrying an ALS-causing mutation.
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Autophagy activators rescue and alleviate pathogenesis of a mouse model with proteinopathies of the TAR DNA-binding protein 43.
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Oligodendrocyte pathology exceeds axonal pathology in white matter in human amyotrophic lateral sclerosis.
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A neurodegeneration-specific gene-expression signature of acutely isolated microglia from an amyotrophic lateral sclerosis mouse model.
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Tamoxifen for amyotrophic lateral sclerosis: A randomized double-blind clinical trial.
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TDP-43 mutations in familial and sporadic amyotrophic lateral sclerosis.
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Oligodendrocyte dysfunction in the pathogenesis of amyotrophic lateral sclerosis.
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Neurotoxic reactive astrocytes are induced by activated microglia.
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Spatiotemporal dynamics of molecular pathology in amyotrophic lateral sclerosis.
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Heterogeneity of cerebral TDP-43 pathology in sporadic amyotrophic lateral sclerosis: Evidence for clinico-pathologic subtypes.
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Phenotypically aberrant astrocytes that promote motoneuron damage in a model of inherited amyotrophic lateral sclerosis.
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Oxidative stress interferes with white matter renewal after prolonged cerebral hypoperfusion in mice.
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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.