ArticleJournal of neuroinflammation2024
Aberrant copper metabolism and hepatic inflammation cause neurological manifestations in a mouse model of Wilson's disease.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Iron and Other Metal Ions in Human Health and Disease.MedComm · 2026Review
- Review
- The ATP7B c.3316 G > A variant is associated with mild subphenotype in Wilson disease: a single-center cohort study.Orphanet journal of rare diseases · 2026Article
- The pathogenesis of liver fibrosis in Wilson's disease: hepatocyte injury and regulation mediated by copper metabolism dysregulation.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Age-associated clinical characteristics andFrontiers in genetics · 2026Article
- Experimental models of hepatic injury in Wilson disease: stage-specific mechanisms and translational applications.Frontiers in immunology · 2026Review
- Osteoporosis in Wilson's disease: A large cohort study highlighting age, sex and skeletal symptoms as key risk factors for clinical surveillance.Orphanet journal of rare diseases · 2025Article
- [Gandou Bushen Decoction Ameliorates Cognitive Impairment in Wilson Disease Model TX Mice by Regulating Melatonin Synthesis via the SIRT3/FOXO3α Pathway].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Concurrent Hyperparathyroidism and Wilson's Disease in a Patient With Methanol Toxicity: A Rare Case Report.Clinical medicine insights. Endocrinology and diabetes · 2025Article
- PKR downregulation prevents copper-induced synaptic dysfunction and cognitive impairment in a murine model of Wilson's disease.Frontiers in neuroscience · 2024Article
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Authors and funding
16 authors.
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Abstract
Pathogenic germline mutations in the P-type copper-transporting ATPase (ATP7B) gene cause Wilson's disease (WD), a hereditary disorder characterized by disrupted copper metabolism. The Arg778Leu (R778L) mutation in exon 8 is prevalent among individuals with WD in East Asia and is associated with more severe phenotypes. In this study, we generated a WD mouse model harboring R778L mutation (R778L mice) using CRISPR/Cas9. R778L mice exhibit a range of pathological characteristics resembling those of patients with WD and the same point mutations, including aberrant copper metabolism, pathological cellular injury, inflammation, and severe hepatic fibrosis. At 3-5 months of age, these mice started to display neurological deficits in motor coordination and cognitive dysfunction, accompanied by increased expression of inflammatory cytokines in the central nervous system. Microglia in the striatum and cortex exhibit significant activation, shorter processes, and decreased branch points. However, the Cu
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