OBJECTIVETo evaluate relationship between ApoE gene polymorphism and coronary heart disease (CHD).

METHODSMeta-analysis was applied with a random-effect model for the collected data.

RESULTSDifference in pooled frequencies, d, of apoE genotypes E3/2, E4/2, E3/3, E4/3 and E4/4 between case and control groups were 2.3%, -0.8%, -8.5%, 10.5% and 0.9%, respectively. Difference in pooled frequencies, d, of apoE alleles epsilon2, epsilon3 and epsilon4 were -1.5%, -4.2% and 5.8%, respectively, with a statistical significance between four groups.

CONCLUSIONSapoE gene polymorphism was involved in coronary heart disease. Persons with apoE E3/3 genotype or epsilon3 allele were not susceptible to CHD, but those with apoE E4/4 genotype or epsilon4 allele had higher risk suffering from CHD than others.

Apolipoproteins E ; genetics ; Coronary Disease ; genetics ; Humans ; Polymorphism, Genetic

Since a decade ago, apolipoprotein (apo) E polymorphism has been focussed as a risk factor for cardiovascular disease. ApoE plays a central role as a receptor ligand for the uptake of lipoproteins from the circulation. There was an agreement on apoE polymorphism being one of the major risk factors for coronary artery disease (CAD) by its effects on lipid profiles. However, the effects of apoE have not been noted in all populations and conflicting results in the risk of CAD have been noted. Recently, in situ expression of apoE on the atherosclerotic plaque has been studied. We, therefore, investigated the effects of apoE genotype on patients with acute coronary syndrome, including unstable angina and acute myocardial infarction, in non-diabetic patients. While we could not find significant risk effects of apoE on coronary artery disease and lipid profiles on simple comparison with the normal control group, we could find significantly decreased frequencies of apo epsilon 3 allele in patients with acute coronary syndrome compared with stable angina patients (77.8% vs 88.8%). We suggest that the apoE genotype could be associated with acute coronary events in CAD and further study with in situ biochemical methods will be needed on the effects of apoE polymorphism on plaque stability.
Apolipoproteins E/genetics* ; Coronary Disease/genetics* ; Genotype ; Human ; Polymorphism (Genetics)/genetics* ; Syndrome

OBJECTIVETo investigate the correlation between the polymorphisms of apolipoprotein E(APOE), the interleukin-1 alpha (IL-1 alpha ) genes and the susceptibility to Alzheimer's disease(AD).

METHODSAssociation study was performed in 114 AD patients and 113 healthy elderly individuals from Chengdu, China. Polymorphisms of APOE and IL-1 alpha genes were analyzed with polymerase chain reaction-restriction fragment length polymorphism.

RESULTSThe frequency of APOE-epsilon 4-carrying genotype in moderate to severe AD patients (28.6%) was higher than that of mild patients (18.5%) and the controls (14.2%), and the difference between moderate to severe AD group and the control group was significant (OR=2.4, 95%CI: 1.1-5.5). The frequency of epsilon 4 was also of significant difference between the group of moderate to severe dementia and the control group (OR=2.6, 95%CI: 1.3-5.3). However, no significant difference in distribution of IL-1 alpha polymorphism between AD patients and controls was observed.

CONCLUSIONThe APOE epsilon 4 allele was associated with moderate to severe AD while no association between the IL-1 alpha gene polymorphism and AD was found.

Alzheimer Disease ; genetics ; Apolipoproteins E ; genetics ; Humans ; Interleukin-1 ; genetics ; Polymorphism, Genetic

Humans ; RNA, Long Noncoding/genetics* ; MicroRNAs/genetics* ; Cell Line, Tumor ; Inflammation/genetics* ; Apolipoproteins E ; Apoptosis

OBJECTIVETo explore the frequency and significance of ApoE gene polymorphisms in patients with sporadic Alzheimer's disease (AD).

METHODSSingle nucleotide polymorphisms of the ApoE gene were analyzed in 32 cases of AD and 26 controls, using PCR and gene sequencing.

RESULTSThe single nucleotide polymorphism of ApoE gene 462C/G was significantly associated with AD (P < 0.05).

CONCLUSIONSThe 462C/G polymorphism might be a specific genotype in Chinese patients with sporadic AD.

Aged ; Alzheimer Disease ; genetics ; Apolipoproteins E ; genetics ; Female ; Genotype ; Humans ; Male ; Polymorphism, Genetic

BACKGROUNDCoronary heart disease (CHD) is a multifactorial disease and is thought to have a polygenic basis. Apolipoprotein E (APOE) gene is one such candidate with its common ε2/ε3/ε4 polymorphism in CHD. In recent years, numerous case-control studies have investigated the relationship of APOE polymorphism with CHD risk. However, the results are confusing.

METHODSTo clarify this point, we undertook a meta-analysis based on 14 published studies including 5746 CHD cases and 19,120 controls. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were assessed for association using a random-effects or fixed-effects model using STATA version 10 (StataCorp LP, College Station, TX, USA).

RESULTSOverall, the analysis showed that carriers of APOE ε2 allele decreased risk for CHD (ε2 allele vs. ε3 allele: OR = 0.82, 95% CI: 0.75-0.90, P < 0.001; ε2 carriers vs. ε3 carriers: OR = 0.81, 95% CI: 0.73-0.89, P < 0.001), compared with those carrying ε3 allele, especially in Caucasian population. However, those with ε4 allele had a significant increased risk for CHD (ε4 allele vs. ε3 allele: OR = 1.34, 95% CI: 1.15-1.57, P < 0.001), especially in Mongoloid population. Potential publication bias was observed in the genetic model of ε4 versus ε3, but the results might not be affected deeply by the publication bias. When we accounted for publication bias using the trim and fill method, the results were not materially alerted, suggesting the stability of our results.

CONCLUSIONSTaken together, our meta-analysis supported a genetic association between APOE gene and CHD. ε4 increased the risk of CHD, whereas ε2 decreased the risk of CHD.

Apolipoproteins E ; genetics ; Coronary Disease ; genetics ; Genetic Predisposition to Disease ; Humans ; Polymorphism, Genetic

Traumatic brain injury (TBI) is defined as an injury caused by a blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain. It is a common emergency and severe case in neurosurgery field. Nowadays, there are more and more evidences showing that TBI, which is apparently similar in pathology and severity in the acute stage, may have different outcomes. The known prognostic factors (such as age, severity of injury and treatments, etc.) explain only part of this variability and the concept of genetic susceptibility of traumatic brain injury has already been accepted by more and more people. It is now demonstrated that genetic polymorphism may play a key role in the susceptibility to TBI, even outcome following TBI. Although there are many genes that may involved in pathophysiological processes influencing TBI, apolipoprotein E gene has become one of the most extensive studied genes in neurotrauma and neurodegenerative disease and seems to take an important part in the neural responses to TBI. In this article, we will review the current understanding of the genetic susceptibility of TBI and the advancements regarding the impact of apolipoprotein E genotype on the severity and/or outcome following TBI.
Animals ; Apolipoproteins E ; genetics ; Brain Injuries ; genetics ; Genetic Predisposition to Disease ; Humans ; Mice

OBJECTIVES: The aim of this study is to examine the cognitive function change related to aging, the incidence of cognitive impairment, and the association between apolipoprotein E polymorphism and cognitive impairment through a follow-up of the elderly with normal cognitive ability at baseline. METHODS: Two hundred and fifteen subjects aged 65 and over were surveyed in February, 1998 (baseline survey), and their cognitive function was assessed again in 2003 (1st follow-up) and the once again in 2006 (2nd follow-up). Ninety one subjects completed all surveys up through the 2nd follow-up and their cognitive function scores using MMSE-K (Korean Version of the Mini-Mental State Examination) and the distribution of apolipoprotein E allele were analyzed. RESULTS: The cognitive function scores decreased with aging and the difference between baseline and the 2nd follow-up scores of the study increased with the age group. The incidence rate of cognitive impairment through an 8-year follow-up was 38.5% and higher in older age groups. Age was the only significant factor for incidence of cognitive impairment, but there was no significant association between apolipoprotein E genotype and incidence of cognitive impairment. CONCLUSIONS: The cognition of the elderly decreased with aging and the association of apolipoprotein E genotype with incidence of cognitive impairment was not significant in this study. To confirm the association between apolipoprotein E polymorphism and incidence of cognitive impairment further studies will be needed.
Aged ; Apolipoproteins E/*genetics ; Cognition/physiology ; Cognition Disorders/etiology/*genetics ; Female ; Humans ; Korea ; Male ; Polymorphism, Genetic

In this study, ultra-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry(UPLC-Q-TOF-MS)-based liver metabolomics approach was used to explore the mechanism of "Trichosanthis Fructus-Allii Macrostemonis Bulbus" in improving atherosclerosis(AS) of mice with apolipoprotein E gene knockout(ApoE~(-/-)). AS mouse model was induced by high-fat diet. The pathological and biochemical indexes such as the histopathological changes, body weight, liver weight, blood lipid level and inflammatory factors in the liver of mice were determined. The metabolic profiling of mice liver samples was performed with UPLC-Q-TOF-MS. Multiple statistical analysis methods including partial least squares discriminant analysis(PLS-DA) and orthogonal partial least squares discriminant analysis(OPLS-DA) were employed to screen and identify biomarkers. The levels of related enzymes including LCAT, sPLA2, EPT1 and ACER1 were detected. The results showed that "Trichosanthis Fructus-Allii Macrostemonis Bulbus" significantly reduced the areas of aortic plaque and fat vacuoles of liver in AS mice and decreased the accumulation of lipid droplets and liver coefficient. "Trichosanthis Fructus-Allii Macrostemonis Bulbus" also regulated the levels of blood lipid and inflammatory injury in the liver. The metabolites of the control group, the model group and the "Trichosanthis Fructus-Allii Macrostemonis Bulbus" group could be distinguished significantly. Fifteen potential biomarkers related to AS were discovered and preliminarily identified, seven of which could be regulated by "Trichosanthis Fructus-Allii Macrostemonis Bulbus" in a trend of returning to normal. Metabolic pathway analysis screened out two major metabolic pathways. "Trichosanthis Fructus-Allii Macrostemonis Bulbus" obviously regulated the levels of LCAT, sPLA2, EPT1 and ACER1. It was inferred that "Trichosanthis Fructus-Allii Macrostemonis Bulbus" could play a major role in AS treatment by regulating glycerophospholipid and sphingolipid metabolism disorders in the liver, with the mechanism probably relating to the intervention of the expression of LCAT, sPLA2, EPT1 and ACER1.
Animals ; Apolipoproteins E/genetics* ; Atherosclerosis/genetics* ; Chromatography, High Pressure Liquid ; Drugs, Chinese Herbal ; Liver ; Metabolomics ; Mice

OBJECTIVE: To evaluate the effects of 12 weeks high intensity interval training(HIIT) on serum lipids profile in patients with dyslipidemia of different apolipoprotein E(ApoE) genotypes. METHODS: Eighty-eight patients with dyslipidemia were screened by fasting blood lipid as subjects. Apolipoprotein E genotypes were detected in oral mucosa of subjects. Serum lipids before and after 12 weeks high intensity interval training were measured to analysis the effect of high intensity interval training on serum lipids. RESULTS: Five genotypes were detected in 88 cases of dyslipidemia. The distributions were ApoE3/3＞ApoE3/4＞ApoE2/3＞ApoE2/2＞ApoE2/4,and allele ε3＞ε2=ε4. Before exercise intervention, the level of total cholesterol in patients with ε4 allele was significant higher than those in patients with ε2 and ε3 (P＜0.01), low density lipoprotein cholesterol in patients with ε4 was significant higher than that of patients with ε2 (P＜0.05), and the other indexes had no significant difference among the groups (P＞ 0.05). After 12 weeks high intensity interval training, the levels of total cholesterol, triglyceride and low density lipoprotein cholesterol were decreased significantly ,while the level of high density lipoprotein cholesterol was increased in those patients with ε3 genotype. For those individuals with ε4 genotype , their serum levels of total cholesterol and low density lipoprotein cholesterol were reduced after 12 weeks high intensity interval training , but there was no changes in serum levels of triglyceride and high density lipoprotein cholesterol. For those individuals with ε2 genotype, there was no significant improvement in serum lipids after 12 weeks high intensity interval training interventions. CONCLUSION The polymorphisms of apolipoprotein E gene resulted in different effects of exercise interventions on serum lipids of dyslipidemia. Twelve weeks high intensity interval training can be used as an intervention method to regulate serum lipids of dyslipidemia with ε3 and ε4 alleles.
Apolipoproteins E ; genetics ; Dyslipidemias ; genetics ; therapy ; Genotype ; High-Intensity Interval Training ; Humans ; Lipids ; blood