title: Myelin and traumatic brain injury: the copper deficiency hypothesis.
abstract: Nearly two million people suffer traumatic brain injury in the US each year. These injuries alter adversely the metabolism of myelin, a major lipid material in brain, both in people and in experimental injuries of animals. A newly discovered and severe human neuropathy from copper deficiency provides evidence that some people in the US are malnourished in copper. As it is well known among copper cognoscenti that it is impossible to synthesize myelin if copper nutriture is inadequate, it seems reasonable to assume that repair will be poor in this situation. Copper status of patients should be evaluated and experiments with injured animals should be repeated with graded doses of copper to determine if copper metabolism is important in this illness.
authors.affiliation: Department of Internal Medicine, University of North Dakota, School of Medicine and Health Sciences, United States; Department of Pharmacology Physiology and Therapeutics, University of North Dakota, School of Medicine and Health Sciences, United States. Electronic address: leslie.klevay@med.und.edu.
authors.forename: Leslie M
authors.initials: LM
authors.lastname: Klevay
mesh_terms: D053898:Biosynthetic Pathways / Q000502:physiology*; D001930:Brain Injuries / Q000209:etiology* / Q000503:physiopathology*; D003300:Copper / Q000172:deficiency* / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D004676:Myelin Basic Protein / Q000134:cerebrospinal fluid; D009186:Myelin Sheath / Q000378:metabolism*
chemical_list: D004676:Myelin Basic Protein; D003300:Copper