ArticleThe American journal of pathology1992
Fragmentation of the Golgi apparatus of motor neurons in amyotrophic lateral sclerosis.
Article in The American journal of pathology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 149 citations in OpenAlex.
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Relationship between promyelocytic leukemia protein nuclear bodies and TAR DNA-binding protein-43 aggregation in spinal anterior horn cells in sporadic amyotrophic lateral sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- The Role of the Golgi Apparatus in Neurodegeneration.Sub-cellular biochemistry · 2026Review
- Three-Dimensional Ultrastructure of the Golgi Apparatus In Vivo: Scanning Electron Microscopy of Osmium-Macerated Mammalian Cells.Sub-cellular biochemistry · 2026Article
- Vesicular trafficking and cell-cell communication in neurodevelopment and neurodegeneration.Frontiers in cell and developmental biology · 2025Review
- Association of APOE genotype and cerebrospinal fluid Aβ and tau biomarkers with cognitive and motor phenotype in amyotrophic lateral sclerosis.European journal of neurology · 2024Article
- Article
- Selecting Genetic Variants and Interactions Associated with Amyotrophic Lateral Sclerosis: A Group LASSO Approach.Journal of personalized medicine · 2022Article
- The Role of GM130 in Nervous System Diseases.Frontiers in neurology · 2021Review
- Retromer stabilization results in neuroprotection in a model of Amyotrophic Lateral Sclerosis.Nature communications · 2020Article
- Human Spinal Motor Neurons Are Particularly Vulnerable to Cerebrospinal Fluid of Amyotrophic Lateral Sclerosis Patients.International journal of molecular sciences · 2020Article
- Review
- Loss of Nuclear TDP-43 Is Associated with Decondensation of LINE Retrotransposons.Cell reports · 2019Article
- ALS Genetics, Mechanisms, and Therapeutics: Where Are We Now?Frontiers in neuroscience · 2019Review
- Multi-Study Proteomic and Bioinformatic Identification of Molecular Overlap between Amyotrophic Lateral Sclerosis (ALS) and Spinal Muscular Atrophy (SMA).Brain sciences · 2018Article
- Control of CNS functions by RNA-binding proteins in neurological diseases.Current pharmacology reports · 2018Article
- Clinical Significance of TDP-43 Neuropathology in Amyotrophic Lateral Sclerosis.Journal of neuropathology and experimental neurology · 2017Article
- Early Golgi Abnormalities and Neurodegeneration upon Loss of Presynaptic Proteins Munc18-1, Syntaxin-1, or SNAP-25.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Loss of the golgin GM130 causes Golgi disruption, Purkinje neuron loss, and ataxia in mice.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Morphometric alterations of Golgi apparatus in Alzheimer's disease are related to tau hyperphosphorylation.Neurobiology of disease · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The Golgi apparatus (complex) is at the center stage of important functions of processing and transport of plasma membrane, lysosomal, and secreted proteins. The involvement of the Golgi apparatus in the pathogenesis of chronic degenerative diseases of neurons is virtually unknown. In the present study, fragmentation and atrophy of the Golgi apparatus of motor neurons in amyotrophic lateral sclerosis (ALS), has been detected with organelle specific antibodies. Approximately 30% of motor neurons in five ALS patients showed a fragmented Golgi apparatus whereas only about 1% of motor neurons from seven controls with neurologic or systemic disease showed a similar change. Morphometric studies are consistent with the hypothesis that the alteration of the Golgi apparatus is an early event in the pathogenesis of the neuronal degeneration in ALS. Immunocytochemical studies with antibodies against alpha tubulin, tau, and phosphorylated subunits of neurofilament polypeptides did not disclose differences in the staining of neurons with fragmented or normal Golgi apparatus, suggesting that the alteration of the organelle is not secondary to a gross lesion of the cytoskeleton. However, these observations do not rule out the hypothesis that the fragmentation of the Golgi apparatus is secondary to subtle changes of the polypeptides involved in the attachment of membranes of the organelle to the cytoskeleton.
Indexed as
Identifiers
1546747PMC1886164W2133086493What 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.