Selenium, selenoprotein P, and Alzheimer's disease: Is there a link?

Nikolay Solovyev, Evgenii Drobyshev, Geir Bjørklund, Yaroslav Dubrovskii, Roman Lysiuk, Margaret P. Rayman

Research output

19 Citations (Scopus)

Abstract

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).

Original languageEnglish
Pages (from-to)124-133
Number of pages10
JournalFree Radical Biology and Medicine
Volume127
DOIs
Publication statusPublished - 2018

Fingerprint

Selenoprotein P
Selenium
Alzheimer Disease
Oxidation-Reduction
Brain
Extravehicular Activity
tau Proteins
Mammals
Amyloid beta-Peptides
Trace Elements
Brain Diseases
Pathology
Cytoskeleton
Mercury
Neurons
Heparin
Copper
Epidemiologic Studies
Glycoproteins
Carrier Proteins

Scopus subject areas

  • Biochemistry
  • Physiology (medical)

Cite this

Solovyev, Nikolay ; Drobyshev, Evgenii ; Bjørklund, Geir ; Dubrovskii, Yaroslav ; Lysiuk, Roman ; Rayman, Margaret P. / Selenium, selenoprotein P, and Alzheimer's disease: Is there a link?. In: Free Radical Biology and Medicine. 2018 ; Vol. 127. pp. 124-133.
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abstract = "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).",
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Selenium, selenoprotein P, and Alzheimer's disease: Is there a link? / Solovyev, Nikolay; Drobyshev, Evgenii; Bjørklund, Geir; Dubrovskii, Yaroslav; Lysiuk, Roman; Rayman, Margaret P.

In: Free Radical Biology and Medicine, Vol. 127, 2018, p. 124-133.

Research output

TY - JOUR

T1 - Selenium, selenoprotein P, and Alzheimer's disease: Is there a link?

AU - Solovyev, Nikolay

AU - Drobyshev, Evgenii

AU - Bjørklund, Geir

AU - Dubrovskii, Yaroslav

AU - Lysiuk, Roman

AU - Rayman, Margaret P.

PY - 2018

Y1 - 2018

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

KW - OXIDATIVE STRESS

KW - PROGRESSIVE CEREBELLOCEREBRAL ATROPHY

KW - PROSTATE-CANCER PREVENTION

KW - HUMAN HEALTH

KW - CEREBROSPINAL-FLUID

KW - LATERAL-SCLEROSIS PATIENTS

KW - COGNITIVE DECLINE

KW - SEVERE NEUROLOGICAL DYSFUNCTION

KW - A-BETA

KW - APOLIPOPROTEIN-E RECEPTOR-2

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U2 - 10.1016/j.freeradbiomed.2018.02.030

DO - 10.1016/j.freeradbiomed.2018.02.030

M3 - Review article

AN - SCOPUS:85043307970

VL - 127

SP - 124

EP - 133

JO - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

SN - 0891-5849

ER -