Author
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Johnson, William |
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Submitted to: Book Chapter
Publication Type: Book / Chapter Publication Acceptance Date: 9/4/2002 Publication Date: 1/1/2005 Citation: Johnson, W.T. 2005. Copper and brain function. In: Lieberman, H.R., Kanarek, R.B., Prasad, C., editors. Nutritional Neuroscience. Boca Raton, FL:CRC Press/Taylor & Francis Group. p. 289-305. Interpretive Summary: Increasing evidence shows that brain development and function are impaired when the brain is deprived of copper either through dietary copper deficiency or through genetic defects in copper transport. A number of copper-dependent enzymes whose activities are lowered by copper deprivation form the basis for the defects in brain function and development associated with copper deficiency. Reductions in the activities of these enzymes that are caused by copper deficiency during brain development are particularly detrimental. Some of the changes in brain structure and function resulting from impaired activity of copper-dependent enzymes during development are irreversible and persist into adulthood. Although copper obtained from the diet is essential for brain development and function, it can also be toxic if cellular levels become excessive. To prevent copper toxicity in the brain, several transport proteins are present that deliver this metal to proteins that require it while at the same time preventing copper from achieving excessive levels. However, mutations in some of the transport proteins impair their ability to regulate copper levels. These mutations are detrimental to brain function and lead to neuropathology because they cause either excessive or abnormally low copper concentrations in the brain. Copper may also cause changes in the brain that are associated with the development of an inherited form of Lou Gehrig's disease and Alzheimer's disease. Technical Abstract: Increasing evidence shows that brain development and function are impaired when the brain is deprived of copper either through dietary copper deficiency or through genetic defects in copper transport. A number of copper-dependent enzymes whose activities are lowered by copper deprivation form the basis for the defects in brain function and development associated with copper deficiency. Reductions in the activities of these enzymes that are caused by copper deficiency during brain development are particularly detrimental. Some of the changes in brain structure and function resulting from impaired activity of copper-dependent enzymes during development are irreversible and persist into adulthood. Although copper obtained from the diet is essential for brain development and function, it can also be toxic if cellular levels become excessive. To prevent copper toxicity in the brain, several transport proteins are present that deliver this metal to proteins that require it while at the same time preventing copper from achieving excessive levels. However, mutations in some of the transport proteins impair their ability to regulate copper levels. These mutations are detrimental to brain function and lead to neuropathology because they cause either excessive or abnormally low copper concentrations in the brain. Copper may also cause changes in the brain that are associated with the development of an inherited form of Lou Gehrig's disease and Alzheimer's disease. |
