Thus, taken together, although the Icelandic heterozygotic carriers do not develop WD, they may exhibit mild abnormali- ties in copper metabolism, as described in the results above. An important limitation is the low power of this study as the sample is small and it would clearly be of interest to investigate bigger groups of heterozygotes for WD to further conﬁrm this trend. Moreover, the heterozygotes in this study are rather young or middle-aged. In a bigger study group it would be relevant to see if neurodegenerative diseases would be more prevalent with rising age in this group than in the general population. The WD patients show similar defects in CP determinations as described earlier from different WD families although the Icelandic mutation of the Wilson gene is unique. Acknowledgments This work was supported by grants from The Memorial Foundation of Helga Jónsdóttir and Sigurlidi Kristjánsson (Medical Division). 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