ArticleMetabolic brain disease2021
Cognitive impairment in stable Wilson disease across phenotype.
Article in Metabolic brain disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- [ModifiedNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Copper loading may affect rat neurobehaviour by impairing mitochondria-associated endoplasmic reticulum membranes in hippocampal neurons.Behavioral and brain functions : BBF · 2025Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Network pharmacology-based approach to understand the effect and mechanism of chrysophanol against cognitive impairment in Wilson disease.Metabolic brain disease · 2024Article
- Comprehensive analysis of the coding and non-coding RNA transcriptome expression profiles of hippocampus tissue in tx-J animal model of Wilson's disease.Scientific reports · 2023Article
- Neuroimaging Correlates of Cognitive Deficits in Wilson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
In Wilson disease (WD), mutations in the gene encoding the ATP7B copper transport protein causes accumulation of copper especially in liver and brain. WD typically presents with hepatic and/or neuropsychiatric symptoms. Impaired cognition is a well-described feature in patients with neurological WD, while the reports on cognition in hepatic WD patients are fewer and less conclusive. We examined cognition in a cohort of WD patients with both phenotypes. In this cross-sectional pilot study, we investigated cognition in 28 stable Danish WD patients by the PortoSystemic Encephalopathy (PSE) and the Continuous Reaction Time (CRT) tests. Half of the patients were female, and their median age was 35.5 years (IQR 24.5). Their phenotype was hepatic in 14 (50%), neurologic in 10 (36%) and mixed in 4 (14%). The duration of treatment was > 2 year in all patients, and their condition was stable as judged by urinary copper excretion, liver enzymes, and clinical assessment. The hepatic patients did not show signs of liver failure. In total, 16 (57%) patients performed worse than normal in the PSE and/or the CRT tests. The two tests were correlated (rho = 0.60, p = 0.0007), but neither correlated with phenotype, MELD-, Child-Pugh score, 24 h-U-Cu, or treatment type. Measurable cognitive impairment was present in more than half of the stable WD patients independent of phenotype. Thus, our data questions the existence of a purely hepatic phenotype.
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