The effects of interactions between selenium and zinc serum concentration and SEP15 and SLC30A3 gene polymorphisms on memory scores in a population of mature and elderly adults

Abstract

Memory deficits are common during aging, but little is known about the impact of environmental and genetic variables on memory. The genes SLC30A3 and SEP15 are, respectively, responsible for transporting zinc and selenium, micronutrients that are neuroprotective agents. The aim of this study was to investigate the effect of nutrigenetic interactions on the memory scores of volunteers more than 50 years old. For this cross-sectional study, 240 individuals were enrolled. Micronutrient dosage was determined using atomic absorption spectrophotometry. The SNPs rs5859, rs5854, and rs561104 in SEP15 and rs73924411 and rs11126936 in SLC30A3 were determined by real-time PCR. The evaluations of verbal and visual memory were performed using the Weschler Memory Scalerevised and the Rey's verbal learning test. A gene versus nutrient interaction was observed for SLC30A3 rs73924411 and zinc concentration. Carriers of the T allele had higher scores for short-term and long-term verbal memories than CC homozygotes only when zinc serum concentration was below the recommended level (p value for the interaction for short-term verbal memory = 0.011, p value for the interaction for long-term verbal memory = 0.039). For SEP15, C carriers of the rs5845 SNP allele had higher verbal learning memory scores than TT homozygotes (0.13 ± 1.13 vs. -1.10 ± 1.20, p = 0.034). Our results suggest the influence of genetic polymorphisms on memory score and identify gene versus nutrient interactions between zinc serum concentration and memory score.

The 811 C/T polymorphism in the 3′ untranslated region of the selenoprotein 15-kDa (Sep15) gene and breast cancer in Caucasian women

“…Of note, the T allele, associated with an increased risk of breast cancer in African women [16], colorectal cancer in Asian men [23], and lung cancer in Caucasians with low Se levels [11], occurs generally more often in African-Americans (31 vs. 7 %) [16]. Therefore, similar to other studies [30,40,41], our results can be impacted by the overall lower presence of the T allele in Caucasians (2-2.4 % TT homozygotes in our data sets).…”

“…A study with 155 healthy women and 106 healthy men from North Dakota (without information about their ethnicity) showed that individuals with the most prevalent (65 %) 811CC genotype had significantly lower buccal cell Se levels than heterozygous individuals (31 %) with the 811TC genotype [42]. Contrarily, in Caucasian individuals from Brazil or New Zealand, the serum Se levels differed not significantly according to the 1125G/A and 811C/T polymorphisms [41,43]. Of note, in most Caucasians, the daily Se intake is below recommended doses but the serum Se levels remain within normal ranges [6,44].…”

Genetic Variations as Modifying Factors to Dietary Zinc Requirements—A Systematic Review

“…The result of the systematic search of the databases is shown in the PRISMA flowchart ( Figure 2 ); eighteen studies matched the inclusion and exclusion criteria. Of these 18 studies, eight were observational cross-sectional [ 21 , 30 , 31 , 32 , 33 , 34 , 35 ], six were case control studies [ 23 , 36 , 37 , 38 , 39 , 40 , 41 ], three were non-randomised clinical control trials ([ 24 , 42 , 43 ], and one was a cross-sectional meta-analysis [ 22 ]. Nine separate genes with 31 SNPs ( Table 1 ), and one study that looked at twins [ 34 ] were identified across the 18 studies.…”

Zinc Signal in Brain Diseases

“…ZnT3 protein levels are decreased across normal ageing in humans, and further decreased in Alzheimer’s disease postmortem brain tissue [ 44 ], together with significant reductions in ZnT3 mRNA levels in disease [ 45 ]. Furthermore, there is an emerging notion that single nucleotide polymorphisms in specific genes, such as that for ZnT3 ( SLC30A3 ), may have an interaction with the nutrient status that impacts upon short- and long-term memory scores in the normal population [ 46 ]. Thus, changes in specific ZnT proteins, or indeed ZIPs or other alterations that alter the normal zinc regulatory apparatus, and that subsequently then precipitate the abnormal homeostasis of zinc within critical brain structures, are likely to alter cognition across both “healthy” and “pathological” ageing.…”