ArticleJournal of Korean medical science2006
Upregulation of proinflammatory cytokines in the fetal brain of the Gaucher mouse.
Article in Journal of Korean medical science, 2006. 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, 54 citations in OpenAlex.
- Transcriptomic signatures in Gaucher disease subtypes: A systems biology perspective.Molecular genetics and metabolism reports · 2025Article
- Combined treatment of Ketogenic diet and propagermanium reduces neuroinflammation in Tay-Sachs disease mouse model.Metabolic brain disease · 2025Article
- Extracellular Vesicles as Tools for Crossing the Blood-Brain Barrier to Treat Lysosomal Storage Diseases.Life (Basel, Switzerland) · 2025Review
- Animal Models for the Study of Gaucher Disease.International journal of molecular sciences · 2023Review
- Exploring Pro-Inflammatory Immunological Mediators: Unraveling the Mechanisms of Neuroinflammation in Lysosomal Storage Diseases.Biomedicines · 2023Review
- Targeting the Complement-Sphingolipid System in COVID-19 and Gaucher Diseases: Evidence for a New Treatment Strategy.International journal of molecular sciences · 2022Review
- Sphingolipid lysosomal storage diseases: from bench to bedside.Lipids in health and disease · 2021Review
- Genetic defects in the sphingolipid degradation pathway and their effects on microglia in neurodegenerative disease.Cellular signalling · 2021Review
- Glycosphingolipids and neuroinflammation in Parkinson's disease.Molecular neurodegeneration · 2020Review
- CRISPR/Cas9 Editing for Gaucher Disease Modelling.International journal of molecular sciences · 2020Article
- Exploring genetic modifiers of Gaucher disease: The next horizon.Human mutation · 2018Review
- Molecular regulations and therapeutic targets of Gaucher disease.Cytokine & growth factor reviews · 2018Review
- Gaucher disease iPSC-derived osteoblasts have developmental and lysosomal defects that impair bone matrix deposition.Human molecular genetics · 2018Article
- Induced Pluripotent Stem Cell Modeling of Gaucher's Disease: What Have We Learned?International journal of molecular sciences · 2017Review
- Osteocyte Alterations Induce Osteoclastogenesis in an In Vitro Model of Gaucher Disease.International journal of molecular sciences · 2017Article
- Neuroinflammatory paradigms in lysosomal storage diseases.Frontiers in neuroscience · 2015Review
- Severe impairment of regulatory T-cells and Th1-lymphocyte polarization in patients with Gaucher disease.JIMD reports · 2015Article
- Mesenchymal stem cells as cellular vectors for pediatric neurological disorders.Brain research · 2014Review
- Clinical and biochemical differences in patients having Parkinson disease with vs without GBA mutations.JAMA neurology · 2013Article
- Immunological cells and functions in Gaucher disease.Critical reviews in oncogenesis · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gaucher disease is caused by a deficiency of glucocerebrosidase. Patients with Gaucher disease are divided into three major phenotypes: chronic nonneuronopathic, acute neuronopathic, and chronic neuronopathic, based on symptoms of the nervous system, the severity of symptoms, and the age of disease onset. The characteristics of patients with acute neuronopathic- and chronic neuronopathic-type Gaucher disease include oculomotor abnormalities, bulbar signs, limb rigidity, seizures and occasional choreoathetoid movements, and neuronal loss. However, the mechanisms leading to the neurodegeneration of this disorder remain unknown. To investigate brain dysfunction in Gaucher disease, we studied the possible role of inflammation in neurodegeneration during development of Gaucher disease in a mouse model. Elevated levels of the proinflammatory cytokines, IL-1alpha, IL-1beta, IL-6, and TNF-alpha, were detected in the fetal brains of Gaucher mice. Moreover, the levels of secreted nitric oxide and reactive oxygen species in the brains of Gaucher mice were higher than in wild-type mice. Thus, accumulated glucocerebroside or glucosylsphingosine, caused by glucocerebrosidase deficiency, may mediate brain inflammation in the Gaucher mouse via the elevation of proinflammatory cytokines, nitric oxide, and reactive oxygen species.
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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.