ArticleJournal of Huntington's disease2012
Genetic Deficiency of Complement Component 3 Does Not Alter Disease Progression in a Mouse Model of Huntington's Disease.
Article in Journal of Huntington's disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- The complement system in neurodegenerative diseases.Clinical science (London, England : 1979) · 2024Article
- The complement system in neurodegenerative and inflammatory diseases of the central nervous system.Frontiers in neurology · 2024Review
- The Complement System in the Central Nervous System: From Neurodevelopment to Neurodegeneration.Biomolecules · 2022Review
- Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021Review
- Neuroimmune crosstalk and evolving pharmacotherapies in neurodegenerative diseases.Immunology · 2021Review
- Precision Medicine in Neurology: The Inspirational Paradigm of Complement Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Complement proteins in unexpected places: why we should be excited, not concerned!F1000Research · 2020Review
- Therapeutic Inhibition of the Complement System in Diseases of the Central Nervous System.Frontiers in immunology · 2019Review
- New tricks for an ancient system: Physiological and pathological roles of complement in the CNS.Molecular immunology · 2018Review
- αB-Crystallin overexpression in astrocytes modulates the phenotype of the BACHD mouse model of Huntington's disease.Human molecular genetics · 2016Article
- Neuroimmunology of Huntington's Disease: Revisiting Evidence from Human Studies.Mediators of inflammation · 2016Review
- The choreography of neuroinflammation in Huntington's disease.Trends in immunology · 2015Review
- Whole gene expression profile in blood reveals multiple pathways deregulation in R6/2 mouse model.Biomarker research · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Several genes and proteins of the complement cascade are present at elevated levels in brains of patients with Huntington's disease (HD). The complement cascade is well characterized as an effector arm of the immune system, and in the brain it is important for developmental synapse elimination. We hypothesized that increased levels of complement in HD brains contributes to disease progression, perhaps by contributing to synapse elimination or inflammatory signaling. We tested this hypothesis in the R6/2 mouse model of HD by crossing mice deficient in complement component 3 (C3), a crucial complement protein found at increased levels in HD brains, to R6/2 mice and monitoring behavioral and neuropathological disease progression. We found no alterations in multiple behavioral assays, weight or survival in R6/2 mice lacking C3. We also quantified the expression of several complement cascade genes in R6/2 brains and found that the large scale upregulation of complement genes observed in HD brains is not mirrored in R6/2 brains. These data show that C3 deficiency does not alter disease progression in the R6/2 mouse model of HD.
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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.