ArticleProceedings of the National Academy of Sciences of the United States of America1998
Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase.
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 50 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.
- Meta-analysis of Genetic Modifiers Reveals Candidate Dysregulated Pathways in Amyotrophic Lateral Sclerosis.Neuroscience · 2019Pooled 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
- 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
- The usage and advantages of several common amyotrophic lateral sclerosis animal models.Frontiers in neuroscience · 2024Review
- The 2022 Lady Estelle Wolfson lectureship on neurofilaments.Journal of neurochemistry · 2022Review
- Article
- The Neglected Genes of ALS: Cytoskeletal Dynamics Impact Synaptic Degeneration in ALS.Frontiers in cellular neuroscience · 2020Review
- Cross talk between SOD1 and the mitochondrial UPR in cancer and neurodegeneration.Molecular and cellular neurosciences · 2019Review
- A motor neuron strategy to save time and energy in neurodegeneration: adaptive protein stoichiometry.Journal of neurochemistry · 2018Article
- Diagnostic and Prognostic Performance of Neurofilaments in ALS.Frontiers in neurology · 2018Review
- Genome-wide RNA-seq of iPSC-derived motor neurons indicates selective cytoskeletal perturbation in Brown-Vialetto disease that is partially rescued by riboflavin.Scientific reports · 2017Article
- Modeling ALS with iPSCs reveals that mutant SOD1 misregulates neurofilament balance in motor neurons.Cell stem cell · 2014Article
- Regulation of CuZnSOD and its redox signaling potential: implications for amyotrophic lateral sclerosis.Antioxidants & redox signaling · 2014Review
- SOD1, an unexpected novel target for cancer therapy.Genes & cancer · 2014Review
- Article
- Genetics of amyotrophic lateral sclerosis: an update.Molecular neurodegeneration · 2013Review
- Distinct changes in synaptic protein composition at neuromuscular junctions of extraocular muscles versus limb muscles of ALS donors.PloS one · 2013Article
- Neurofilaments at a glance.Journal of cell science · 2012Review
- Identification of pharmacological targets in amyotrophic lateral sclerosis through genomic analysis of deregulated genes and pathways.Current genomics · 2012Article
- The complex molecular biology of amyotrophic lateral sclerosis (ALS).Progress in molecular biology and translational science · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
To investigate the role of neurofilaments in motor neuron disease caused by superoxide dismutase (SOD1) mutations, transgenic mice expressing a amyotrophic lateral sclerosis-linked SOD1 mutant (SOD1(G37R)) were mated with transgenic mice expressing human neurofilament heavy (NF-H) subunits. Unexpectedly, expression of human NF-H transgenes increased by up to 65%, the mean lifespan of SOD1(G37R) mice. Microscopic examination corroborated the protective effect of NF-H protein against SOD1 toxicity. Although massive neurodegeneration occurred in 1-yr-old mice expressing SOD1(G37R) alone, spinal root axons and motor neurons were remarkably spared in doubly SOD1(G37R);NF-H-transgenic littermates.
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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.