ArticleNeuropsychiatric disease and treatment2009
Ceruloplasmin and superoxide dismutase (SOD1) in heterozygotes for Wilson disease: A case control study.
Article in Neuropsychiatric disease and treatment, 2009. 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, 7 citations in OpenAlex.
- SOD1-Related Cerebellar Ataxia and Motor Neuron Disease: Cp Variant as Functional Modifier?Cerebellum (London, England) · 2024Article
- Wilson's Disease-Genetic Puzzles with Diagnostic Implications.Diagnostics (Basel, Switzerland) · 2023Review
- Transcriptome analysis of sinensetin-treated liver cancer cells guided by biological network analysis.Oncology letters · 2021Article
- Alagille syndrome and Wilson disease in siblings: a diagnostic conundrum.Canadian journal of gastroenterology = Journal canadien de gastroenterologie · 2012Article
- Ceruloplasmin and iron in Alzheimer's disease and Parkinson's disease: a synopsis of recent studies.Neuropsychiatric disease and treatment · 2012Article
- Middle-aged heterozygous carriers of Wilson's disease do not present with significant phenotypic deviations related to copper metabolism.Journal of genetics · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At the time of this study, there were five known patients with Wilson disease (WD) in Iceland. The mutation, a 7-bp deletion in exon 7 on chromosome 13 for WD, is only known in Iceland. In twenty healthy Icelandic heterozygotes for WD and their age- and gender-matched controls, copper concentration in plasma, ceruloplasmin (CP) concentration, CP oxidative activity and CP-specific oxidative activity in serum and superoxide dismutase (SOD1) activity in erythrocytes were determined. The same determinations were done on the five WD patients. There was no significant difference in these parameters between the heterozygotes and the controls, although an inclination toward lower CP determinations and higher SOD1 activity in the heterozygotes was noted. As expected the WD patients were low on the copper and CP parameters, but their SOD1 activity was within the upper normal range. In conclusion, the CP parameters and SOD1 activity are within the normal range in Icelandic heterozygotes for WD, although with a trend toward mild dyshomeostasis. This may indicate subclinical copper retention in the heterozygotes, but a bigger study group is needed to confirm this.
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