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dc.contributor.authorAlecksynas, Tess
dc.contributor.authorTownsend, Eric
dc.contributor.authorZhu, Angela
dc.contributor.authorBrabetz, Barbara
dc.date.accessioned2016-05-11T21:17:44Z
dc.date.available2016-05-11T21:17:44Z
dc.date.issued2016
dc.identifier.urihttp://hdl.handle.net/1951/67548
dc.description.abstractThe absence of functional ceruloplasminferroxidase activity impairs the body’s ability to export iron out of its tissues. The resulting accumulation of iron in the cells result in tissue damage and ultimately health concerns such as aceruloplasminaemia, Parkinsonism, and multiple system atrophy (Miyajima, 2003) (Motta, 2009).While not directly affected by mutations in the CP gene, individuals with copper-transport diseases such as Wilson disease and Menkes’diseasemay exhibit low levels of Ceruloplasmin (Mercer, 2001).en_US
dc.language.isoen_USen_US
dc.subjectCeruloplasminLCSH
dc.subjectIron in the bodyLCSH
dc.subjectBrain—Localization of functionsLCSH
dc.titleHeavy Metal on the Brain: CeruloplasminTessen_US
dc.typeLearning Objecten_US
dc.typePresentationen_US


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