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: Contribution to journalReview articlepeer-review

78 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 - 1 Nov 2018
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Amyloid-beta
  • Brain
  • Human studies
  • Model studies
  • Neurodegeneration
  • Oxidative stress
  • Redox regulation
  • Selenium
  • Selenoprotein P
  • Supplementation
  • Trace elements

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