|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
APOE ε4 (OR = 4.482, P = 0.004), the RS2305421 GG genotype (adjusted OR = 4.397, P = 0.015), and the RS10498633 GT genotype (adjusted OR = 2.375, P = 0.028) were associated with a higher score on the ABC (Aβ plaque score, Braak NFT stage, and CERAD neuritic plaque score) dementia scale.
|
30783964 |
2019 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
We apply the method to Alzheimer's data from the Rush University Religious Orders Study and Memory and Aging Project, where as proof of principle we find highly significant associations with the APOE gene, in both the "structural zero" and "count" parameters, when applied to a zero-inflated NPs count outcome.
|
30353568 |
2019 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Enhancing ABCA1 activity to reduce ApoE and ABCA1 aggregation is a potential therapeutic strategy for the prevention of ApoE4 aggregation-driven pathology.<b>SIGNIFICANCE STATEMENT</b> ApoE protein plays a key role in the formation of amyloid plaques, a hallmark of Alzheimer's disease (AD).
|
31641056 |
2019 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
In this model, AP formation does not depend on [Aβ]c. The present interpretation of the AH, unifying the pathogenetic theories for IAD and NIAD, will explain why AP and APOE4 may be observed in healthy aging and why they are not the cause of AD.
|
30883346 |
2019 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Aβ lesions closely correlate with the ApoE4 allele and appear as the earliest event in the development of senile plaques.
|
30099348 |
2018 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
An increased expression of GMF in APs and neurofibrillary tangles in the AD brain, and the co-localization of GMF and ApoE4 in APs suggest that GMF and ApoE4 together should be contributing to the neuropathological changes associated with AD.
|
29172001 |
2018 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Regression analyses found that increased ISD was associated with increased NFT pathology (β= 10.93, SE = 3.82, p = 0.004), but not with DPs (β= 1.33, SE = 8.85, p = 0.88) or NPs (β= 14.64, SE = 8.45, p = 0.08) after adjusting for age at death, gender, education, APOE ɛ4 status, and clinical diagnosis.
|
28453479 |
2017 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
The three cases with apolipoprotein E ε4 haplotype showed scattered β-amyloid plaques in the overlying gray matter, but not the two cases with apolipoprotein E ε3/3 genotype.
|
27885490 |
2017 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
After adjusting for age at death, education, gender, Braak stage, and APOE ɛ4 carrier status, the presence of NPs was associated with lower performance in the cognitive domains of Global Cognition (p = 0.002), Episodic Memory (p = 0.03), Semantic Memory (p = 0.009), and Visuospatial performance (p = 0.006), while DPs showed no association with any cognitive domain examined.
|
27540968 |
2016 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
The patients were apoE genotyped and the density of β-amyloid senile plaques, neuritic plaques and neurofibrillary tangles was estimated in the cortex and hippocampus.
|
25898889 |
2015 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
APOE [Latin Small Letter Open E]4 is a major risk factor for late-onset Alzheimer disease, a progressive neurodegenerative disorder that affects memory, thinking, behavior, and emotion as a result of the excessive buildup and decreased clearance of β-amyloid proteins resulting in the appearance of neuritic plaques and neurofibrillary tangles.
|
23715207 |
2015 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Of the 13 APOE4 carriers with minimal neuritic plaques, 6 individuals (46.2%) had Braak stages III to VI ratings and met neuropathologic criteria for other dementia-related diseases.
|
26302353 |
2015 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
The relationship between β-amyloid plaques and dementia in the oldest-old may vary by APOE genotype.
|
23474043 |
2013 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
In age- and APOE-adjusted analyses, the minor G-allele of rs2774276, previously linked to elevated cholesterol, associated with late-stage burnt out SP among women and early non-neuritic SP among men.
|
22390463 |
2012 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Cholesterol and LDL relate to neuritic plaques and to APOE4 presence but not to neurofibrillary tangles.
|
21244352 |
2011 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
In multivariate analyses (age- and APOE-adjusted), non-neuritic SP were associated with the high-CRP TA-genotype (3.0% prevalence) of rs3091244 and CA-genotype (10.8%) of rs3093075 compared to common genotypes.
|
21831326 |
2011 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Nondemented APOE e4 carriers over age 60 have a higher burden of total parenchymal and vascular amyloid neuropathology than NC, but no difference in neuritic plaque and NFT pathology.
|
20153809 |
2010 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
The loads of IHC/Abeta, silver stained neuritic plaques (NP) and neurofibrillary tangles (NFT) were significantly higher in subjects carrying the Apolipoprotein E e4 allele.
|
18346114 |
2009 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
This neuropathological study used both silver staining and A beta immunohistochemistry in brain tissue microarrays, including SP coverage and NFT counts from frontal cortex and hippocampus, and APOE genotyping, and was performed on a consecutive prospective series of 603 subjects (aged between 0 and 97 years) of an unselected population living outside of institutions.
|
19557866 |
2009 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
In a linear regression model, AP percentage area was associated with age (p < 0.0001) and APOE epsilon4 allele (p < 0.0001), but not with CW score (p = 0.70) or gender (p = 0.11).
|
19521084 |
2009 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Possession of the CTSD T allele does not increase the risk of developing AD per se, but has a modulating effect on the pathogenesis of the disorder by increasing, in concert with the APOE e4 allele, the amount of Abeta deposited as senile plaques in the brain in the form of Abeta40.
|
16543533 |
2006 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Diffuse plaques seen during early stages of AD differ from neuritic plaques in later stages both with respect to the length of the Abeta peptides and the presence of other proteins, e.g., apolipoprotein-E (apoE).
|
16195918 |
2005 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
There was a trend toward association between APOE genotype and amyloid angiopathy (p = 0.08), and epsilon4 was associated with neuritic SP burden, but not NFT.
|
16043796 |
2005 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Analyses of covariance controlling for age at death, dementia severity (Clinical Dementia Rating score), and APOE4 allele indicated that diabetics had significantly fewer neuritic plaques (p =.008) and NFTs (p =.047) in the cerebral cortex than did nondiabetics.
|
15933386 |
2005 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
LB stage V had higher stages of neurofibrillary tangle and senile plaque involvement and also had a higher frequency of apolipoprotein E epsilon4.
|
15290899 |
2004 |