TY - JOUR
T1 - Selenium, selenoprotein P, and Alzheimer's disease
T2 - is there a link?
AU - Solovyev, Nikolay
AU - Drobyshev, Evgenii
AU - Bjørklund, Geir
AU - Dubrovskii, Yaroslav
AU - Lysiuk, Roman
AU - Rayman, Margaret P.
N1 - Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2018/11/1
Y1 - 2018/11/1
N2 - The essential trace element, selenium (Se), is crucial to the brain but it may be potentially neurotoxic, depending on dosage and speciation; Se has been discussed for decades in relation to Alzheimer's disease (AD). Selenoprotein P (SELENOP) is a secreted heparin-binding glycoprotein which serves as the main Se transport protein in mammals. In vivo studies showed that this protein might have additional functions such as a contribution to redox regulation. The current review focuses on recent research on the possible role of SELENOP in AD pathology, based on model and human studies. The review also briefly summarizes results of epidemiological studies on Se supplementation in relation to brain diseases, including PREADViSE, EVA, and AIBL. Although mainly positive effects of Se are assessed in this review, possible detrimental effects of Se supplementation or exposure, including potential neurotoxicity, are also mentioned. In relation to AD, various roles of SELENOP are discussed, i.e. as the means of Se delivery to neurons, as an antioxidant, in cytoskeleton assembly, in interaction with redox-active metals (copper, iron, and mercury) and with misfolded proteins (amyloid-beta and hyperphosphorylated tau-protein).
AB - The essential trace element, selenium (Se), is crucial to the brain but it may be potentially neurotoxic, depending on dosage and speciation; Se has been discussed for decades in relation to Alzheimer's disease (AD). Selenoprotein P (SELENOP) is a secreted heparin-binding glycoprotein which serves as the main Se transport protein in mammals. In vivo studies showed that this protein might have additional functions such as a contribution to redox regulation. The current review focuses on recent research on the possible role of SELENOP in AD pathology, based on model and human studies. The review also briefly summarizes results of epidemiological studies on Se supplementation in relation to brain diseases, including PREADViSE, EVA, and AIBL. Although mainly positive effects of Se are assessed in this review, possible detrimental effects of Se supplementation or exposure, including potential neurotoxicity, are also mentioned. In relation to AD, various roles of SELENOP are discussed, i.e. as the means of Se delivery to neurons, as an antioxidant, in cytoskeleton assembly, in interaction with redox-active metals (copper, iron, and mercury) and with misfolded proteins (amyloid-beta and hyperphosphorylated tau-protein).
KW - Alzheimer's disease
KW - Amyloid-beta
KW - Brain
KW - Human studies
KW - Model studies
KW - Neurodegeneration
KW - Oxidative stress
KW - Redox regulation
KW - Selenium
KW - Selenoprotein P
KW - Supplementation
KW - Trace elements
UR - http://www.scopus.com/inward/record.url?scp=85043307970&partnerID=8YFLogxK
U2 - 10.1016/j.freeradbiomed.2018.02.030
DO - 10.1016/j.freeradbiomed.2018.02.030
M3 - Review article
C2 - 29481840
AN - SCOPUS:85043307970
SN - 0891-5849
VL - 127
SP - 124
EP - 133
JO - Free Radical Biology and Medicine
JF - Free Radical Biology and Medicine
ER -