The risks of free copper in the body and the development of useful anticopper drugs.
OBJECTIVE
To review the toxicity and risks of free copper in Wilson's disease, Alzheimer's disease, other disease of neurodegeneration, and cognitive loss in the general population. We will also review the anticopper drugs and how lowering free copper levels with an anticopper drug inhibits fibrosis, inflammation, and autoimmunity.


RESULTS
Some exciting recent work indicates that free copper levels are increased in Alzheimer's disease, and copper may be involved in disease pathogenesis, opening the way to possible therapy of Alzheimer's disease with anticopper drugs. Copper may also be involved in other diseases of neurodegeneration. A very exciting recent study indicts high intake of copper, mostly from copper supplements, in conjunction with a high-fat diet in more rapid cognitive decline in the general population. Other data indicate that even low levels of copper in drinking water, perhaps similar to copper supplements, bypasses the liver, enters the circulation, increases the blood-brain penetration of copper, and may cause damage.


CONCLUSIONS
Some of the implications are that Alzheimer's disease and other diseases of neurodegeneration and fibrotic, inflammatory, and autoimmune diseases may be treatable by lowering the availability of free copper. People in the general population may wish to take steps to lower their free copper levels and, in particular, to abstain from taking copper supplements and ingesting significant amounts of copper in drinking water.
Brewer
George J
GJ
Department of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan 48109-5720, USA. brewergj@umich.edu
D000544:Alzheimer Disease / Q000139:chemically induced / Q000188:drug therapy / Q000517:prevention & control; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D015551:Autoimmunity / Q000187:drug effects / Q000502:physiology; D003300:Copper / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D005355:Fibrosis / Q000378:metabolism / Q000517:prevention & control; D006527:Hepatolenticular Degeneration / Q000139:chemically induced / Q000188:drug therapy / Q000517:prevention & control; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000517:prevention & control; D008982:Molybdenum / Q000627:therapeutic use; D019636:Neurodegenerative Diseases / Q000139:chemically induced* / Q000188:drug therapy* / Q000517:prevention & control; D010396:Penicillamine / Q000627:therapeutic use; D014266:Trientine / Q000627:therapeutic use
D020533:Angiogenesis Inhibitors; D003300:Copper; D008982:Molybdenum; D010396:Penicillamine; D014266:Trientine