Abstract
Humans consume about 1 mg of copper daily, an amount thought adequate for most needs. Genetic, environmental, or physiological alterations can impose a higher copper set point, increasing risk for copper-limited pathophysiology. Humans express about a dozen proteins that require copper for function (cuproenzymes). Limitation in the activity of cuproenzymes can explain the pleiotropic effect of copper deficiency. However, for most of the salient features of human copper deficiency, the precise molecular mechanisms are unknown. This is true for the two most common clinical features, hypochromic anemia and adult onset peripheral neuropathy/ataxia, a condition described frequently in the last decade due to multiple etiologies. The challenge for future scientists will be to identify the mechanisms underlying the pathophysiology of copper deficiency so appropriate screening and treatment can occur. The need for a strong copper biomarker to aid in this screening is critical.
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