Serúlóplasmín og járn. Tengsl við Alzheimersjúkdóm og Parkinsonsjúkdóm
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Issue Date
2012-10
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Ceruloplasmin (Cp) and iron in connection with Parkinson's disease (PD) and Alzheimer's disease (AD)Citation
Læknablaðið 2012, 98(10):531-7Abstract
Ceruloplasmin, a multi-copper oxidase with four active copper atoms, oxidizes Fe2+ to Fe3+ and concomittantly fully reduces oxygen to water. The oxygenation of iron is a requisite for transferrin transport of iron and keeping noxious Fe2+ low. In the central nervous system (CNS) Cp is mostly localized in end feet of astrocytes surrounding capillaries and attached by a glycosylphosphatidylinositol-anchor. In aceruloplasminaemia, a rare recessive hereditary disease, complete loss of Cp is accompanied by disorders of iron metabolism and lesions in CNS and outside. In PD Cp concentration and oxidative activity in serum are significantly lowered with iron deposits and lesions in substantia nigra and basal ganglia. Changes in Cp-genes might be causative in these disorders. By inducing neuromelanin synthesis Cp may protect neurons in substantia nigra. In AD Cp activity in serum, but not concentration, is significantly lowered. Changes in Cp-genes have not been verified in AD. Total amounts of iron are not increased in AD brains although iron deposits and cortical lesions are numerous. Total copper is significantly lowered in AD brains. This may result in defective synthesis of Cp and other copper enzymes. - In conclusion, the defective Cp activity, associated with iron disorders, is seemingly of importance in PD and also in AD with other copper enzyme defects possibly involved.Serúlóplasmín (Cp) er svokallaður multi-kopar oxídasi, sem in vivo oxar Fe2+ í Fe3+ og afoxar jafnframt súrefni að fullu í vatn. Cp tryggir að Fe3+ geti bundist transferríni og að magn hvarfgjarns Fe2+ haldist í lágmarki. Í miðtaugakerfinu er það einkum bundið örmum stirnufrumna með glýkósýlfosfatidýlinósítól-tengi í námunda við æðar. Í Cp eru fjögur virk koparatóm og er festing þeirra óskylt ferli myndunar próteinhluta ensímsins. Í Cp-þurrð í blóði (aserúlóplasmínemía) er alger vöntun á Cp og áberandi járnraskanir í miðtaugakerfinu og utan þess. Í Parkinsonsjúkdómi (PD) er bæði Cp-þéttni og oxunarvirkni í sermi minnkuð, samfara áberandi járnsöfnun í svartsviðið í miðheila. Cp gæti hamlað uppkomu PD með því að binda járn í neurómelaníni og varna oxunarskemmdum í orkukornum taugunga í svartsviði. Ríkur erfðaþáttur er í PD og breytingar í Cp-genum gætu tengst erfðamynstrinu. Í Alzheimersjúkdómi (AD) er oxunarvirkni Cp minnkuð í sermi, en ekki þéttni þess. Breytingar í Cp-genum virðast ekki tengjast AD. Við AD eru bæði járnraskanir og vöntun á kopar í heilanum. Koparskortur gæti valdið truflun á myndun virks Cp auk annarra koparensíma í heila. Ætla má að trufluð Cp-virkni, og þar með raskaður járnbúskapur, skipti máli við PD og við AD ásamt hugsanlega truflunum á öðrum koparensímum.
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