|
Alzheimer Disease, Late Onset
|
|
0.030 |
GeneticVariation
|
BEFREE |
We propose that these structural and functional changes underlie the observed added risk for AD development in carriers of apoE4[L28P].
|
24644280 |
2014 |
|
Alzheimer Disease, Late Onset
|
|
0.030 |
GeneticVariation
|
BEFREE |
The minor allele of p.L28P, which was in complete linkage disequilibrium (D' = 1) with the far more common APOE ϵ4 allele, showed no association with LOAD (P = 0.75) independent of the APOE ϵ4 allele. p.V236E was significantly associated with a marked reduction in risk of LOAD (P = 7.5 × 10⁻⁰⁵; OR = 0.10, 0.03 to 0.45).
|
24607147 |
2014 |
|
Alzheimer Disease, Late Onset
|
|
0.030 |
GeneticVariation
|
BEFREE |
Compared to E3/3 and E3/2 genotypes, the risk of developing AD associated with the genotypes carrying the e(*)4 allele, the well-established risk allele for AD onset, was observed to be high (OR=3.16; 95% CI=1.62-6.20; P=0.0009), but the risk associated with genotypes carrying the Leu28-->Pro mutation was higher still (OR=10.95; 95% CI=1.25-95.75; P=0.015).
|
12498968 |
2003 |
|
Coronary heart disease
|
|
0.020 |
GeneticVariation
|
BEFREE |
The aim of this study was to investigate the individual or combined effects of PPARA-L162V, PPARG-C161T and APOE polymorphisms on hyperlipidemia in coronary heart disease (CHD) patients.
|
23583468 |
2013 |
|
Coronary heart disease
|
|
0.020 |
GeneticVariation
|
BEFREE |
Effects of a frequent apolipoprotein E isoform, ApoE4Freiburg (Leu28-->Pro), on lipoproteins and the prevalence of coronary artery disease in whites.
|
10323784 |
1999 |
|
Childhood Neuroblastoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
Specifically, apoE4[L28P] promoted the cellular uptake of extracellular amyloid β peptide 42 (Aβ42) by human neuroblastoma SK-N-SH cells as well as by primary mouse neuronal cells and led to increased formation of intracellular reactive oxygen species that persisted for at least 24 h. Furthermore, lipoprotein particles containing apoE4[L28P] induced intracellular reactive oxygen species formation and reduced SK-N-SH cell viability.
|
24644280 |
2014 |
|
Central neuroblastoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
Specifically, apoE4[L28P] promoted the cellular uptake of extracellular amyloid β peptide 42 (Aβ42) by human neuroblastoma SK-N-SH cells as well as by primary mouse neuronal cells and led to increased formation of intracellular reactive oxygen species that persisted for at least 24 h. Furthermore, lipoprotein particles containing apoE4[L28P] induced intracellular reactive oxygen species formation and reduced SK-N-SH cell viability.
|
24644280 |
2014 |
|
Neuroblastoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
Specifically, apoE4[L28P] promoted the cellular uptake of extracellular amyloid β peptide 42 (Aβ42) by human neuroblastoma SK-N-SH cells as well as by primary mouse neuronal cells and led to increased formation of intracellular reactive oxygen species that persisted for at least 24 h. Furthermore, lipoprotein particles containing apoE4[L28P] induced intracellular reactive oxygen species formation and reduced SK-N-SH cell viability.
|
24644280 |
2014 |
|
Hyperlipidemia
|
|
0.010 |
GeneticVariation
|
BEFREE |
The aim of this study was to investigate the individual or combined effects of PPARA-L162V, PPARG-C161T and APOE polymorphisms on hyperlipidemia in coronary heart disease (CHD) patients.
|
23583468 |
2013 |
|
Coronary Artery Disease
|
|
0.010 |
GeneticVariation
|
BEFREE |
Effects of a frequent apolipoprotein E isoform, ApoE4Freiburg (Leu28-->Pro), on lipoproteins and the prevalence of coronary artery disease in whites.
|
10323784 |
1999 |
|
Coronary Arteriosclerosis
|
|
0.010 |
GeneticVariation
|
BEFREE |
Effects of a frequent apolipoprotein E isoform, ApoE4Freiburg (Leu28-->Pro), on lipoproteins and the prevalence of coronary artery disease in whites.
|
10323784 |
1999 |