ArticleNeurochemical research2016
Cerebrospinal Fluid from Sporadic Amyotrophic Lateral Sclerosis Patients Induces Mitochondrial and Lysosomal Dysfunction.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Receptor-mediated mitophagy: a new target of neurodegenerative diseases.Frontiers in neurology · 2025Review
- Role of mitochondrial quality control in neurodegenerative disease progression.Frontiers in cellular neuroscience · 2025Review
- Inhibition of NF-κB with an Analog of Withaferin-A Restores TDP-43 Homeostasis and Proteome Profiles in a Model of Sporadic ALS.Biomedicines · 2024Article
- HERV-K (HML-2) Envelope Protein Induces Mitochondrial Depolarization and Neurotoxicity via Endolysosome Iron Dyshomeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Review
- BNIP3L/NIX-mediated mitophagy: molecular mechanisms and implications for human disease.Cell death & disease · 2021Review
- ALS-CSF-induced structural changes in spinal motor neurons of rat pups cause deficits in motor behaviour.Experimental brain research · 2021Article
- 40 Years of CSF Toxicity Studies in ALS: What Have We Learnt About ALS Pathophysiology?Frontiers in molecular neuroscience · 2021Review
- Molecular Mechanisms of Lysosome and Nucleus Communication.Trends in biochemical sciences · 2020Review
- Defining novel functions for cerebrospinal fluid in ALS pathophysiology.Acta neuropathologica communications · 2020Review
- Human Spinal Motor Neurons Are Particularly Vulnerable to Cerebrospinal Fluid of Amyotrophic Lateral Sclerosis Patients.International journal of molecular sciences · 2020Article
- Transmission of ALS pathogenesis by the cerebrospinal fluid.Acta neuropathologica communications · 2020Article
- Calcium Dyshomeostasis and Lysosomal CaCells · 2019Review
- Cerebrospinal Fluid from Patients with Sporadic Amyotrophic Lateral Sclerosis Induces Degeneration of Motor Neurons Derived from Human Embryonic Stem Cells.Molecular neurobiology · 2019Article
- Proteomics Approaches for Biomarker and Drug Target Discovery in ALS and FTD.Frontiers in neuroscience · 2019Review
- A Systematic Review of Suggested Molecular Strata, Biomarkers and Their Tissue Sources in ALS.Frontiers in neurology · 2019Review
- Multi-Study Proteomic and Bioinformatic Identification of Molecular Overlap between Amyotrophic Lateral Sclerosis (ALS) and Spinal Muscular Atrophy (SMA).Brain sciences · 2018Article
- Sporadic amyotrophic lateral sclerosis (SALS) - skeletal muscle response to cerebrospinal fluid from SALS patients in a rat model.Disease models & mechanisms · 2018Article
- Inhibition of Drp1/Fis1 interaction slows progression of amyotrophic lateral sclerosis.EMBO molecular medicine · 2018Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our laboratory, we have developed (1) an in vitro model of sporadic Amyotrophic Lateral Sclerosis (sALS) involving exposure of motor neurons to cerebrospinal fluid (CSF) from sALS patients and (2) an in vivo model involving intrathecal injection of sALS-CSF into rat pups. In the current study, we observed that spinal cord extract from the in vivo sALS model displayed elevated reactive oxygen species (ROS) and mitochondrial dysfunction. Quantitative proteomic analysis of sub-cellular fractions from spinal cord of the in vivo sALS model revealed down-regulation of 35 mitochondrial proteins and 4 lysosomal proteins. Many of the down-regulated mitochondrial proteins contribute to alterations in respiratory chain complexes and organellar morphology. Down-regulated lysosomal proteins Hexosaminidase, Sialidase and Aryl sulfatase also displayed lowered enzyme activity, thus validating the mass spectrometry data. Proteomic analysis and validation by western blot indicated that sALS-CSF induced the over-expression of the pro-apoptotic mitochondrial protein BNIP3L. In the in vitro model, sALS-CSF induced neurotoxicity and elevated ROS, while it lowered the mitochondrial membrane potential in rat spinal cord mitochondria in the in vivo model. Ultra structural alterations were evident in mitochondria of cultured motor neurons exposed to ALS-CSF. These observations indicate the first line evidence that sALS-CSF mediated mitochondrial and lysosomal defects collectively contribute to the pathogenesis underlying sALS.
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