ArticleProceedings of the National Academy of Sciences of the United States of America1998
Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 234 citations in OpenAlex.
- Pooled it
- High-throughput screening of ALS patient iPSC-derived spinal motor neurons identifies novel compounds that increase neurofilament light chain expression.SLAS discovery : advancing life sciences R & D · 2026Article
- Wdfy3-dependent autophagy impairment recapitulates presymptomatic neurodegenerative signatures in mice.Scientific reports · 2026Article
- Long-term atorvastatin improves cognitive function by modulating SIRT2-mediated dynamic transition of NFL lysine 272 crotonylation to ubiquitination in naturally aging rats.Cell death discovery · 2025Article
- KIF5A regulates axonal repair and time-dependent axonal transport of SFPQ granules and mitochondria in human motor neurons.bioRxiv : the preprint server for biology · 2024Article
- The usage and advantages of several common amyotrophic lateral sclerosis animal models.Frontiers in neuroscience · 2024Review
- The Role of Mitophagy in Various Neurological Diseases as a Therapeutic Approach.Cellular and molecular neurobiology · 2023Review
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Phenotypic correlates of serum neurofilament light chain levels in amyotrophic lateral sclerosis.Frontiers in aging neuroscience · 2023Article
- The protective role of exercise against age-related neurodegeneration.Ageing research reviews · 2022Review
- Article
- Amyloid Oligomers: A Joint Experimental/Computational Perspective on Alzheimer's Disease, Parkinson's Disease, Type II Diabetes, and Amyotrophic Lateral Sclerosis.Chemical reviews · 2021Review
- Neurofilament Light Chain as Biomarker for Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.Frontiers in neuroscience · 2021Review
- Disrupted neuronal trafficking in amyotrophic lateral sclerosis.Acta neuropathologica · 2019Review
- The Role of Exercise as a Non-pharmacological Therapeutic Approach for Amyotrophic Lateral Sclerosis: Beneficial or Detrimental?Frontiers in neurology · 2019Review
- Copy Number Variations in Amyotrophic Lateral Sclerosis: Piecing the Mosaic Tiles Together through a Systems Biology Approach.Molecular neurobiology · 2018Review
- Diagnostic and Prognostic Performance of Neurofilaments in ALS.Frontiers in neurology · 2018Review
- Neurofilament depletion improves microtubule dynamics via modulation of Stat3/stathmin signaling.Acta neuropathologica · 2016Article
- Calpastatin inhibits motor neuron death and increases survival of hSOD1(G93A) mice.Journal of neurochemistry · 2016Article
- A Case for Microtubule Vulnerability in Amyotrophic Lateral Sclerosis: Altered Dynamics During Disease.Frontiers in cellular neuroscience · 2016Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in superoxide dismutase 1 (SOD1), the only proven cause of amyotrophic lateral sclerosis (ALS), provoke disease through an unidentified toxic property. Neurofilament aggregates are pathologic hallmarks of both sporadic and SOD1-mediated familial ALS. By deleting NF-L, the major neurofilament subunit required for filament assembly, onset and progression of disease caused by familial ALS-linked SOD1 mutant G85R are significantly slowed, while selectivity of mutant-mediated toxicity for motor neurons is reduced. In NF-L-deleted animals, levels of the two remaining neurofilament subunits, NF-M and NF-H, are markedly reduced in axons but are elevated in motor neuron cell bodies. Thus, while neither perikaryal nor axonal neurofilaments are essential for SOD1-mediated disease, the absence of assembled neurofilaments both diminishes selective vulnerability and slows SOD1(G85R) mutant-mediated toxicity to motor neurons.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.