ApoE gene polymorphisms and metals and their interactions with cognitive function.

OBJECTIVE: To analyze the relationship between plasma metal elements, ApoE gene polymorphisms and the interaction between the two and impaired cognitive function in elderly population. METHOD: A stratified sample was drawn according to the age of the study population, and 911 subjects were included. Baseline information and health indicators were obtained, and cognitive function status was assessed by health examination, a general questionnaire and Mini-Mental Status Examination. Plasma metal elements were measured, and SNP typing was performed. Binary logistic regression was used to analyze the factors influencing cognitive function status and the association between the SNP genetic pattern of the ApoE gene and cognitive function. RESULTS: The differences in gene frequencies and genotype frequencies of the ApoE rs7412 and rs7259620 genotype frequencies were statistically different between the cognitive impairment group and the control group (P < 0.05). statistically differences were found for the codominant model in rs7412-TT compared with the CC genotype (OR = 3.112 (1.159-8.359), P = 0.024) and rs7259620-AA compared with the GG genotype (OR = 1.588 (1.007-2.504), P = 0.047). Statistically differences were found in the recessive models rs7412-TT compared with (CC + CT) (OR = 2.979 (1.112-7.978), P = 0.030), rs7259620-AA compared with (GG + GA), and rs405509-GG compared with (TT + TG) (OR = 1.548(1.022-2.344), P = 0.039) all of which increased the risk of developing cognitive impairment. The differences in plasma Fe, Cu, and Rb concentrations between the case and control groups were significant (P < 0.05). The regression results showed that the plasma Cd concentrations in the Q1 range was a protective factor for cognitive function compared with Q4 (0.510 (0.291-0.892), P = 0.018). Furthermore, there was a multiplicative interaction between the codominant and recessive models for the Q2 concentrations of Cd and the rs7259620 loci, and the difference was significant, indicating increased risk of developing cognitive impairment (codominant model OR = 3.577 (1.496-8.555), P = 0.004, recessive model OR = 3.505 (1.479-8.307), P = 0.004). There was also a multiplicative interaction between Cd and the recessive model at the rs405509 loci, and the difference was significant, indicating increased risk of developing cognitive impairment (OR = 3.169 (1.400-7.175), P = 0.006). CONCLUSION: The ApoE rs7412, rs7259620 and rs405509 loci were associated with cognitive impairment in the elderly population, and there was an interaction between plasma metalloid Cd and the rs7259620 and rs405509 loci that increased the risk of cognitive impairment in the elderly population.

The Relationship Between APOE Gene Polymorphism and In-stent Restenosis After Stenting at the Beginning of the Vertebral Artery.

OBJECTIVE: To retrospectively investigate the relationship between apolipoprotein E (APOE) gene polymorphism and in-stent restenosis (ISR) after stenting at the beginning of the vertebral artery. METHODS: The study included 155 patients who successfully underwent stenting at the beginning of the vertebral artery and had postoperative digital subtraction angiography or computed tomography angiography. Based on the follow-up results, they were divided into the restenosis (ISR) group and non-restenosis (non-ISR) group. The clinical information and APOE genotypes of both groups were analyzed. A binary logistic regression model was used to analyze independent risk factors for ISR. RESULTS: After 1 year of follow-up, 49 (31.6%) patients had ISR and 106 (68.4%) did not. Binary logistic regression analysis showed that serum low-density lipoprotein cholesterol (LDL-C), serum lipoprotein-related phospholipase A2 (Lp-PLA2), and E3/E4 genotype were independent risk factors for ISR after stenting at the beginning of the vertebral artery. In addition, the LDL-C level of patients with the E3/E4 genotype was higher compared with the E3/E3 genotype group (P < 0.05). CONCLUSIONS: APOE gene polymorphism is associated with ISR, and the E3/E4 genotype is an independent risk factor for ISR after stenting at the beginning of the vertebral artery. Further genetic studies can identify risk genotypes to facilitate the early prediction and identification of high-risk patients with ISR.

Relationship Between the Apolipoprotein E Genotype and LDL Particle Size in Patients With Obstructive Sleep Apnea.

Obstructive sleep apnea (OSA) is associated with dyslipidemia and increased cardiovascular risk. We assessed the effects of apolipoprotein E ( APOE) genotype on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particle size and lipid subclasses (separated by gradient gel electrophoresis) in patients with OSA. Stable patients (n = 181) prospectively recruited underwent full polysomnography. Both LDL particle size and LDL I proportion were reduced from ∊3∊3 homozygotes to ∊2 carriers and to ∊4 carriers (analysis of variance: P = .024; P = .040, respectively); carriers of the ∊4 allele of the APOE genotype had significantly lower LDL particle size and LDL I proportion compared to ∊3∊3 homozygotes ( P < .05 for both comparisons). Insulin resistance increased from patients with no OSA to those with mild-moderate and to those with severe OSA ( P < .001). In multivariate analysis, LDL size was independently predicted by APOE genotype, male gender, and the presence of metabolic syndrome (MetS; P = .001, P = .020, P = .027, respectively). The HDL particle size was not affected by APOE genotype. Our data demonstrate that both the ∊4 APOE genotype and MetS are independently related to smaller LDL size in patients with OSA.

The relationship of the apolipoprotein E gene polymorphism in Turkish Type 2 Diabetic Patients with and without diabetic foot ulcers.

AIMS: The aim of this study was to investigate the association between Apolipoprotein E (ApoE) gene polymorphism in the development of diabetic foot ulcers in Type 2 diabetes Turkish patients. MATERIALS AND METHODS: The ApoE genotypes were determined retrospectively in 50 patients with diabetic foot and 50 without diabetic foot and a control group of 50 healthy individuals. RESULTS: The genotype ApoE distribution did differ between the control group (E2E3 44%, E3E3 38%, E3E4 18%) and Type 2 Diabetic Patients (E2E3 6%, E3E3 81%, E3E4 16%) (p<0.001). The genotype ApoE distribution did not differ between Type 2 Diabetic Patients group (E2E3 4%, E3E3 86%, E3E4 4%) and diabetic foot ulcers (E2E3 8%, E3E3 76%, E3E4 16%) (p>0.05). The frequency of the E2,E3,E4 allele in between the control group and Type 2 Diabetic Patients were no similar for the groups (E2 22%, E3 69%, E4 9% and E2 3%, E3 90.5%, E4 6.5%, respectively) (p<0.001). The frequency of the E2-E4 allele in between the Type 2 Diabetic Patients and diabetic foot ulcers were similar for the groups (E2 2%, E3 93%, E4 5% and E2 4%, E3 88%, E4 8%, respectively) (p>0.05). CONCLUSIONS: The gene polymorphism of ApoE and E3 allele are a risk factor for diabetes, but gene polymorphism of ApoE is not an independent risk factor for diabetic foot. Lack of association between ApoE gene polymorphism and Type 2 diabetic foot ulcers might be due to ethnic differences.

Association among oxidized LDL levels, MnSOD, apolipoprotein E polymorphisms, and cardiovascular risk factors in a south Brazilian region population

Oxidized LDL (ox-LDL) is involved in the initiation and progression of atherosclerosis. Many factors can affect the LDL oxidation such as oxidative stress. The present study tested whether ox-LDL levels would be associated with apolipoprotein E (APOE), manganese superoxide dismutase (MnSOD) Ala16Val polymorphisms, and classic cardiovascular risk factors. ox-LDL levels were measured by thiobarbituric acid-reactive substances and both polymorphisms were determined by polymerase chain reaction/restriction fragment length polymorphism in a sample of 252 subjects (70 men, 182 women, mean age, 54-85 years). Subjects with ox-LDL >or=0.5 nmol/mg apoprotein were considered the high level group (HLG, N = 82) and subjects with ox-LDL <0.5 nmol/mg apoprotein were considered the expected level group (ELG, N = 170). Classic risk factors were also evaluated. The results showed that diabetes mellitus was more prevalent in HLG, whereas other cardiovascular risk factors were similar between groups. The APOE genotype frequencies did not differ between HLG and ELG subjects. However, AA genotype from MnSOD polymorphism was more frequent in ELG (chi(2) = 8.48; P = 0.014). AV and VV subjects from ELG present highest ox-LDL levels (OR = 3.61; CI95% = 1.42-9.17) than AA. Additional analysis did not find gene-gene interactions associated with ox-LDL levels. Multivariate analysis showed that diabetes and the MnSOD polymorphism were independent factors associated with higher ox-LDL levels in HLG. The results suggest that an important framework on modulation of the redox status influenced by genetic polymorphisms could affect the cardiovascular homeostasis.