Abstract
Selenoproteins play important roles in antioxidant mechanisms, and are thus hypothesised to have some involvement in the pathology of certain types of dementia. Mild cognitive impairment (MCI) and Alzheimer's disease (AD) are both thought to involve impaired biological activity of certain selenoproteins. Previously, supplementation with a selenium-rich Brazil nut (Bertholletia excelsa) has shown potential in reducing cognitive decline in MCI patients, and could prove to be a safe and effective nutritional approach early in the disease process to slow decline. Here, we have conducted a pilot study that examined the effects of a range of single nucleotide polymorphisms (SNPs) in genes encoding the selenoproteins glutathione peroxidase (GPX1) and selenoprotein P (SEPP) in response to selenium supplementation via dietary Brazil nuts, including selenium status, oxidative stress parameters and GPX1 and SEPP gene expression. Our data suggest that GPX1 Pro198Leu rs1050450 genotypes may differentially affect the selenium status and GPx activity. Moreover, rs7579 and rs3877899 SNPs in SEPP gene, as well as GPX1 rs1050450 genotypes can influence the expression of GPX1 and SEPP mRNA in response to Brazil nuts intake. This small study gives cause for larger investigations into the role of these SNPs in both the selenium status and response to selenium dietary intake, especially in chronic degenerative conditions like MCI and AD.
Highlights
Despite significant research, strategies to slow the progression of cognitive decline and the onset of dementia are lacking
We have conducted a pilot study that examined the effects of a range of single nucleotide polymorphisms (SNPs) in genes encoding the selenoproteins glutathione peroxidase (GPX1) and selenoprotein P (SEPP) in response to selenium supplementation via dietary Brazil nuts, including selenium status, oxidative stress parameters and glutathione peroxidase 1 (GPX1) and SEPP gene expression
Rs7579 and rs3877899 SNPs in SEPP gene, as well as GPX1 rs1050450 genotypes can influence the expression of GPX1 and SEPP mRNA in response to Brazil nuts intake
Summary
Strategies to slow the progression of cognitive decline and the onset of dementia are lacking. It is estimated that the number of people living with dementia, such as Alzheimer’s disease which accounts as the main type, will reach 65.7 million in 2030 and nearly double in 2050.1 Addressing dementia prior to the onset of clinical symptoms is as important as the development of therapeutics for postdiagnostic use. Several risk factors linked to lifestyle have been identified, which include dietary-related conditions such as midlife obesity, diabetes and hypertension, and if they were to some people do not exhibit the explicit clinical symptoms of dementia, they may develop cognitive impairment beyond what would be expected for normal ageing. Single nucleotide polymorphisms (SNPs) in amyloid precursor protein (APP) and presenilin-1 (PSEN1) and 2 (PSEN2) genes have been implicated in the predisposition of early-onset familial AD;[8,9,10,11] and SNPs in the genes encoding apolipoprotein E (APOE) and α2-macroglobulin (A2M) are associated with late-onset AD.[12,13] Genome wide association studies (GWAS) have identified several additional genes that appear to
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