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205 records – page 1 of 21.

Age-dependent association of apolipoprotein E genotype with coronary and aortic atherosclerosis in middle-aged men: an autopsy study.

https://arctichealth.org/en/permalink/ahliterature201193
Source
Circulation. 1999 Aug 10;100(6):608-13
Publication Type
Article
Date
Aug-10-1999
Author
E. Ilveskoski
M. Perola
T. Lehtimäki
P. Laippala
V. Savolainen
J. Pajarinen
A. Penttilä
K H Lalu
A. Männikkö
K K Liesto
T. Koivula
P J Karhunen
Author Affiliation
Medical School, University of Tampere, Tampere University Hospital, Finland. ei46478@uta.fi
Source
Circulation. 1999 Aug 10;100(6):608-13
Date
Aug-10-1999
Language
English
Publication Type
Article
Keywords
Age Factors
Alcoholism - mortality
Alleles
Aorta, Abdominal - pathology
Aorta, Thoracic - pathology
Aortic Diseases - epidemiology
Apolipoprotein E3
Apolipoprotein E4
Apolipoproteins E - genetics
Arteriosclerosis - epidemiology - genetics - pathology
Autopsy
Body mass index
Cardiovascular Diseases - mortality
Cause of Death
Comorbidity
Coronary Artery Disease - epidemiology - genetics - pathology
Finland - epidemiology
Gene Frequency
Genetic Predisposition to Disease
Genotype
Heterozygote
Humans
Male
Middle Aged
Obesity - epidemiology
Violence
Abstract
Apolipoprotein E (apoE) polymorphism is one of the genetic determinants of serum cholesterol values. The apoE epsilon4 allele has been associated with advanced coronary heart disease (CHD) diagnosed by angiography, but the role of the apoE genotype in atherosclerosis has not been confirmed at vessel-wall level, nor is any age-dependent effect of the apoE genotype on the development of CHD known.
The right and left anterior descending coronary arteries (RCA and LAD) and the aorta from 700 male autopsy cases (Helsinki Sudden Death Study) in 1981-1982 and 1991-1992 (average age 53 years, range 33 to 70 years) were stained for fat, and all areas covered with fatty streaks, fibrotic plaques, and complicated lesions were measured. In the RCA and LAD, the apoE genotype was significantly associated with the area of total atherosclerotic lesions in men
PubMed ID
10441097 View in PubMed
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Age-dependent interaction of apolipoprotein E gene with eastern birthplace in Finland affects severity of coronary atherosclerosis and risk of fatal myocardial infarction--Helsinki Sudden Death Study.

https://arctichealth.org/en/permalink/ahliterature119352
Source
Ann Med. 2013 May;45(3):213-9
Publication Type
Article
Date
May-2013
Author
Petri Tyynelä
Sirkka Goebeler
Erkki Ilveskoski
Jussi Mikkelsson
Markus Perola
Terho Lehtimäki
Pekka J Karhunen
Author Affiliation
School of Medicine, University of Tampere, Tampere, Finland. petri.tyynela@uta.fi
Source
Ann Med. 2013 May;45(3):213-9
Date
May-2013
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
Alleles
Apolipoproteins E - genetics
Coronary Artery Disease - mortality
Coronary Vessels - pathology
Death, Sudden, Cardiac - epidemiology
Finland - epidemiology
Genotype
Humans
Male
Middle Aged
Multivariate Analysis
Out-of-Hospital Cardiac Arrest - mortality
Plaque, Atherosclerotic - pathology
Residence Characteristics
Risk assessment
Risk factors
Severity of Illness Index
Abstract
Mortality from coronary heart disease (CHD) has been constantly higher in eastern late settlement regions compared to western early settlements in Finland, unrelated to classical risk factors. In line with this, eastern birthplace was an age-dependent predictor of severe coronary atherosclerosis and pre-hospital sudden coronary death among male residents of Helsinki. We investigated a possible interaction of apolipoprotein E (APOE) gene with birthplace on the risk of myocardial infarction (MI) and coronary atherosclerosis.
APOE genotypes were analyzed in the Helsinki Sudden Death Study series comprising out-of-hospital deaths among males aged 33-70 years (n = 577), who were born in high (east, n = 273) or low (west, n = 304) CHD mortality area.
Eastern-born men = 55 years carried 30% more often (P = 0.017) and older men 40% less often (P = 0.022) the APOE ?4 allele compared to western-born men (P = 0.003 for birthplace-by-age interaction). In multivariate analysis, the ?4 allele associated with the risk of out-of-hospital MI (odds ratio 2.58; 95% CI 1.20-5.55; P = 0.016) only in eastern-born men and with advanced atherosclerosis in both regions of origin, respectively.
Birthplace-bound risk of CHD was age-dependently modified by APOE ?4 allele, suggesting genetic differences in CHD susceptibility between early and late settlement regions in Finland and providing one explanation for the eastern high mortality.
PubMed ID
23110590 View in PubMed
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Aggregation of lipoprotein and inflammatory parameters in families with a history of premature myocardial infarction: the Tallinn myocardial infarction study.

https://arctichealth.org/en/permalink/ahliterature154200
Source
Clin Chem Lab Med. 2008;46(11):1602-8
Publication Type
Article
Date
2008
Author
Katrin Aasvee
Elvira Kurvinen
Jouko Sundvall
Matti Jauhiainen
Inna Tur
Author Affiliation
Department of Chronic Disease Prevention, National Institute for Health Development, Tallinn, Estonia. katrin.aasvee@tai.ee
Source
Clin Chem Lab Med. 2008;46(11):1602-8
Date
2008
Language
English
Publication Type
Article
Keywords
Acute-Phase Proteins - metabolism
Adolescent
Adult
Age Factors
Apolipoprotein A-I - blood
Apolipoproteins B - blood
Apolipoproteins E - genetics
C-Reactive Protein - metabolism
Child
Cholesterol - blood
Cholesterol, HDL - blood
Cholesterol, LDL - blood
Family Health
Female
Finland
Humans
Lipoprotein(a) - blood
Lipoproteins - blood
Male
Middle Aged
Myocardial Infarction - blood - genetics
Polymorphism, Genetic
Risk factors
Sex Factors
Triglycerides - blood
Abstract
The offspring of individuals with a history of premature myocardial infarction are at increased risk of premature coronary attacks. The aim of this study was to determine parent/offspring associations of coronary risk factors in families affected by premature myocardial infarction and to compare these to corresponding control families.
The cohort of cases consisted of 71 male survivors of myocardial infarction and their 128 descendants (aged 7-18 years). As control families, 85 randomly selected healthy males with their 66 descendants were investigated. Besides traditional risk factors, serum high sensitive C-reactive protein (hsCRP), apolipoprotein (apo) E phenotypes and lipoprotein(a) were analyzed.
In the offspring of the patients, fibrinogen and atherogenic lipoprotein parameters were higher than in the corresponding controls, but hsCRP, lipoprotein(a) and anthropometric data did not differ between the groups. The adult-offspring positive correlations were detected in fibrinogen and in almost all measured lipoprotein fractions in the affected families; amongst the controls, the association was observed only for triglyceride levels. Multiple logistic regression analysis demonstrated independent association of offspring apoB, apoA-I and fibrinogen levels with a family history of premature myocardial infarction.
The most informative predictors of future coronary attacks during childhood are apoB-100 and apoB/apoA-I ratio; serum hsCRP and lipoprotein(a) do not have predictive value in childhood.
PubMed ID
19012525 View in PubMed
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Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men.

https://arctichealth.org/en/permalink/ahliterature10634
Source
Circulation. 1999 Aug 17;100(7):723-8
Publication Type
Article
Date
Aug-17-1999
Author
S. Boquist
G. Ruotolo
R. Tang
J. Björkegren
M G Bond
U. de Faire
F. Karpe
A. Hamsten
Author Affiliation
Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Hospital, Stockholm, Sweden.
Source
Circulation. 1999 Aug 17;100(7):723-8
Date
Aug-17-1999
Language
English
Publication Type
Article
Keywords
Alcohol drinking - epidemiology
Apolipoproteins B - blood
Apolipoproteins E - genetics
Area Under Curve
Arteriosclerosis - epidemiology - ultrasonography
Blood pressure
Body constitution
Carotid Artery, Common - ultrasonography - ultrastructure
Carotid Stenosis - epidemiology - ultrasonography
Chylomicrons - blood
Dietary Fats - pharmacokinetics
Eating - physiology
Fasting - blood
Genotype
Homeostasis
Humans
Insulin - blood
Lipids - blood
Lipoproteins - blood
Lipoproteins, LDL Cholesterol - blood
Lipoproteins, VLDL - blood
Male
Middle Aged
Proinsulin - blood
Reference Values
Research Support, Non-U.S. Gov't
Smoking - epidemiology
Sweden - epidemiology
Triglycerides - blood
Tunica Intima - ultrastructure
Abstract
BACKGROUND: Alimentary lipemia has been associated with coronary heart disease and common carotid artery intima-media thickness (IMT). This study was designed to investigate the relations of subclasses of postprandial triglyceride-rich lipoproteins (TRLs) with IMT. METHODS AND RESULTS: Ninety-six healthy 50-year-old men with an apolipoprotein (apo) E3/E3 genotype underwent an oral fat tolerance test and B-mode carotid ultrasound examination. The apo B-48 and apo B-100 contents of each fraction of TRLs were determined as a measure of chylomicron remnant and VLDL particle concentrations. In the fasting state, LDL cholesterol (P
PubMed ID
10449694 View in PubMed
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Allele frequencies of apolipoprotein E gene polymorphisms in the protein coding region and promoter region (-491A/T) in a healthy Norwegian population.

https://arctichealth.org/en/permalink/ahliterature190719
Source
Hum Biol. 2002 Feb;74(1):137-42
Publication Type
Article
Date
Feb-2002
Author
Kumar T
Liestøl K
Maehlen J
Hiorth A
Jettestuen E
Lind H
Brorson S-H
Author Affiliation
Department of Pathology, Ulleväl Hospital, Oslo, Norway.
Source
Hum Biol. 2002 Feb;74(1):137-42
Date
Feb-2002
Language
English
Publication Type
Article
Keywords
Adult
Alleles
Apolipoproteins E - genetics
Chi-Square Distribution
Female
Gene Frequency
Genotype
Humans
Male
Norway - epidemiology
Polymerase Chain Reaction
Polymorphism, Genetic
Promoter Regions, Genetic
Abstract
This study examines the distribution of apolipoprotein E (APOE) alleles in a population of healthy male and female Norwegians (n = 798) below the age of 40. The -491A/T polymorphism of the promoter region of the APOE gene was also examined. A seminested polymerase chain reaction was applied in the genotyping. The results showed that the E3 allele had the highest frequency (0.744), followed by E4 (0.198) and E2 (0.058). The APOE frequencies found in this study differ significantly from those obtained in earlier Norwegian APOE phenotypings. The allele frequencies in the -491 site of the promoter region were 0.845 for the A allele and 0.155 for the T allele. The genotype frequency was highest for AA (0.707), followed by AT (0.277) and TT (0.016). Moreover, the A allele was in linkage disequilibrium to E4.
PubMed ID
11931575 View in PubMed
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Allelic association but only weak evidence for linkage to the apolipoprotein E locus in late-onset Swedish Alzheimer families.

https://arctichealth.org/en/permalink/ahliterature211853
Source
Am J Med Genet. 1996 May 31;67(3):306-11
Publication Type
Article
Date
May-31-1996
Author
L. Liu
C. Forsell
L. Lilius
K. Axelman
E H Corder
L. Lannfelt
Author Affiliation
Karolinska Institute, Department of Clinical Neuroscience, Huddinge, Sweden.
Source
Am J Med Genet. 1996 May 31;67(3):306-11
Date
May-31-1996
Language
English
Publication Type
Article
Keywords
Age of Onset
Aged
Alleles
Alzheimer Disease - genetics - metabolism
Apolipoprotein E2
Apolipoprotein E3
Apolipoprotein E4
Apolipoproteins E - genetics
Female
Genetic Linkage
Humans
Male
Middle Aged
Sweden
Abstract
An association between the epsilon 4 allele of the apolipoprotein E gene (APOE) and late-onset Alzheimer's disease (AD) was recently demonstrated. In order to confirm the association and to gauge the ability of standard genetic linkage methods to identify susceptibility genes, we investigated 15 Swedish late-onset Ad families. We found an association of familial AD to the APOE epsilon 4 allele (P = 0.01) but no indication of linkage to the APOE region using 2-point linkage analysis, and only weak evidence using the affected pedigree-member (APM) method. Our results confirm an APOE epsilon 4 association with late-onset familial AD and indicate that susceptibility genes can easily be missed when using standard lod score and APM genetic linkage analysis.
PubMed ID
8725748 View in PubMed
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Analyzing age-specific genetic effects on human extreme age survival in cohort-based longitudinal studies.

https://arctichealth.org/en/permalink/ahliterature121617
Source
Eur J Hum Genet. 2013 Apr;21(4):451-4
Publication Type
Article
Date
Apr-2013
Author
Qihua Tan
Rune Jacobsen
Mette Sørensen
Lene Christiansen
Torben A Kruse
Kaare Christensen
Author Affiliation
Institute of Public Health, University of Southern Denmark, Odense C, Denmark. qtan@health.sdu.dk
Source
Eur J Hum Genet. 2013 Apr;21(4):451-4
Date
Apr-2013
Language
English
Publication Type
Article
Keywords
Aged, 80 and over
Alleles
Apolipoproteins E - genetics
Cohort Studies
Denmark
Female
Genotype
Humans
Longevity - genetics
Longitudinal Studies
Male
Models, Genetic
Population - genetics
Abstract
The analysis of age-specific genetic effects on human survival over extreme ages is confronted with a deceleration pattern in mortality that deviates from traditional survival models and sparse genetic data available. As human late life is a distinct phase of life history, exploring the genetic effects on extreme age survival can be of special interest to evolutionary biology and health science. We introduce a non-parametric survival analysis approach that combines population survival information with individual genotype data in assessing the genetic effects in cohort-based longitudinal studies. Our approach is characterized by non-parametric analysis of late age survival to capture the observed pattern of mortality deceleration and frailty modeling to account for individual heterogeneity in unobserved frailty. The method is applied to ApoE genotype data in the Danish 1905 birth cohort to estimate effect of the e4 allele. Our results revealed an age-specific relative risk of the allele that increases nonlinearly with age and non-proportional patterns in hazard of death for carriers and non-carriers of the allele, suggesting that the e4 mutation preserves its deleterious effect that progressively affect human survival even at extreme ages.
Notes
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PubMed ID
22892531 View in PubMed
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APOE and AGT in the Finnish p.Arg133Cys CADASIL population.

https://arctichealth.org/en/permalink/ahliterature273253
Source
Acta Neurol Scand. 2015 Dec;132(6):430-4
Publication Type
Article
Date
Dec-2015
Author
M. Siitonen
K. Mykkänen
F. Pescini
S. Rovio
H. Kääriäinen
M. Baumann
M. Pöyhönen
M. Viitanen
Source
Acta Neurol Scand. 2015 Dec;132(6):430-4
Date
Dec-2015
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Aged
Aged, 80 and over
Angiotensinogen - genetics
Apolipoproteins E - genetics
CADASIL - epidemiology - genetics
Female
Finland - epidemiology
Gene Frequency
Humans
Male
Middle Aged
Migraine Disorders - etiology
Mutation
Phenotype
Polymorphism, Single Nucleotide - genetics
Receptors, Notch - genetics
Stroke - epidemiology
Young Adult
Abstract
CADASIL is an inherited systemic small vessel disease, the affected status of brain vessels leading to subcortical vascular dementia. The defective gene is NOTCH3 in which over 230 different pathogenic mutations have been identified. The clinical course of CADASIL is highly variable even within families. Previous studies have shown that additional genetic factors modify the phenotype.
Altogether, 134 Finnish CADASIL patients with p.Arg133Cys mutation were analysed for possible associations between the apolipoprotein E (APOE) genotype, angiotensinogen (AGT) p.Met268Thr polymorphism or neutral p.Ala202Ala NOTCH3 polymorphism and earlier first-ever stroke or migraine.
We found no association between the APOE genotypes, AGT polymorphism, NOTCH3 polymorphism and earlier first-ever stroke or migraine.
The APOE, AGT and NOTCH3 polymorphism did not modify the onset of strokes or migraine in our CADASIL sample, which is one of the largest mutationally homogenous CADASIL populations published to date. International collaboration, pooled analyses and genomewide approaches are warranted to identify the genetic factors that modify the highly variable CADASIL phenotype.
PubMed ID
25819272 View in PubMed
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205 records – page 1 of 21.