Selenium attenuates Aβ production and Aβ-induced neuronal death

Gwon, A-Ryeong; Park, Jong‐Sung; Park, Jun Hyung; Baik, Sang‐Ha; Jeong, Hye-Young; Hyun, Dong Hoon; Park, Kye Won; Jo, Dong-Gyu

doi:10.1016/j.neulet.2009.12.035

Cited by 47 publications

(24 citation statements)

References 32 publications

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“…Lower concentrations are necessary for cell survival and growth, whereas higher concentrations inhibit growth and induce cell death (Selenius et al 2010;Zeng and Combs 2008). It has been determined that Se protects neurons against insults relevant to the pathogenesis of neurodegenerative disorders (Gwon et al 2010). Selenite sodium induces neurodegeneration at lM level in primary cultured cortical neurons through an apoptotic pathway, and the apoptotic cells increase proportionally to the concentration and the exposure time of sodium selenite (Xiao et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Effects of Selenoprotein W gene expression by selenium involves regulation of mRNA stability in chicken embryos neurons

et al. 2012

Biometals

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Selenium (Se) and Selenoprotein W (SelW) plays a pivotal role in the brain development, function, and degeneration and that SelW expression in the brain may be affected by Se. However, the mechanism which Se regulates the SelW gene expression in neurons remains to be unclear. To investigate the effects of the SelW gene expression and mRNA stability induced by Se, primary cultured chicken embryos neurons derived from 8-day-old chick embryo cerebral hemispheres were treated with 10(-9)-10(-5) mol/l Se as selenite for 3, 6, 12, 24 or 48 h, respectively. The morphology and viability of Neurons was detected. The SelW mRNA expression level and mRNA half-life was examined in Se-treated neurons. The relative low concentrations of Se enhanced the neurite outgrowth, increased the SelW mRNA levels and elevated the mRNA half-life of chick embryo neurons. In contrast, the high concentrations of Se presented neurotoxic to neurons, decreased the SelW mRNA levels and reduced the mRNA half-life of neuronal cells. These results suggest that the alteration of post-transcriptional stabilization of SelW mRNA is an important mechanism of Se-induced the elevation or reduction of the SelW expression level in chick embryo neurons.

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Section: Discussionmentioning

confidence: 99%

Effects of Selenoprotein W gene expression by selenium involves regulation of mRNA stability in chicken embryos neurons

et al. 2012

Biometals

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“…In particular, Se treatment has been reported to attenuate γ-secretase activity, reduce Aβ production, increase GPx activity, and prevent Aβ-induced neuronal death [125, 126]. Additional cell culture studies have also found that treatment with Se, in the form of sodium selenate (Na 2 SeO 4 ), increased the activity of the serine-threonine phosphatase PP2A and reduced tau phosphorylation [127, 128].…”

Section: Selenium Selenoproteins and Neurological Diseasementioning

confidence: 99%

Selenoproteins in Nervous System Development and Function

Pitts

Byrns

Ogawa-Wong

et al. 2014

Biol Trace Elem Res

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Selenoproteins are a distinct class of proteins that are characterized by the co-translational incorporation of selenium (Se) in the form of the 21st amino acid selenocysteine. Selenoproteins provide a key defense against oxidative stress, as many of these proteins participate in oxidation-reduction reactions neutralizing reactive oxygen species, where selenocysteine residues act as catalytic sites. Many selenoproteins are highly expressed in the brain and mouse knockout studies have determined that several are required for normal brain development. In parallel with these laboratory studies, recent reports of rare human cases with mutations in genes involved in selenoprotein biosynthesis have described individuals with an assortment of neurological problems that mirror those detailed in knockout mice. These deficits include impairments in cognition and motor function, seizures, hearing loss, and altered thyroid metabolism. Additionally, due to the fact that oxidative stress is a key feature of neurodegenerative disease, there is considerable interest in the therapeutic potential of selenium supplementation for human neurological disorders. Studies performed in cell culture and rodent models have demonstrated that selenium administration attenuates oxidative stress, prevents neurodegeneration, and counters cell signaling mechanisms known to be dysregulated in certain disease states. However, there is currently no definitive evidence in support of selenium supplementation to prevent and/or treat common neurological conditions in the general population. It appears likely, that in humans, supplementation with selenium may only benefit certain subpopulations, such as those that are either selenium-deficient or possess genetic variants that affect selenium metabolism.

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“…These data further suggest that alterations in the Se concentration and its related enzymes may play a role in the etiopathogenesis of AD. Se has been associated to the reduction of Aβ production and of Aβ induction of neuronal death in cells culture [11]. In animal models of AD, Se prevented oxidative damage and modulated the cholinergic system [12,13].…”

Section: Introductionmentioning

confidence: 99%