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apoe4
268 studies tagged apoe4, dated 1993-09-01 to 2026-10-27. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
268 studies carry this tag.
Date range
1993 to 2026
Top journals
- Neuron 11
- The Journal of neuroscience : the official journal of the Society for Neuroscience 9
- International journal of molecular sciences 8
- Alzheimer's & dementia : the journal of the Alzheimer's Association 7
- bioRxiv 6
169 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Emerging evidence suggests that these morphological changes reflect functional alterations that affect disease.
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Alzheimer's disease (AD) is the most common type of dementia and, after age, the greatest risk factor for developing AD is the allelic variation of apolipoprotein E (ApoE), with homozygote carriers of the ApoE4 allele having an up to 12-fold greater risk of developing AD than noncarriers.
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Apolipoprotein E (apoE), a 34 kDa circulating glycoprotein of 299 amino acids, predominantly synthesised in the liver, associates with triglyceride-rich lipoproteins to mediate the clearance of their remnants after enzymatic lipolysis in the circulation.
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46/100
CSF-sLR11 concentrations were higher in patients with AD than controls (adjusted for sLR11 using phospholipid).
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Alzheimer's disease (AD) is one of the most devastating neurodegenerative diseases.
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The apolipoprotein E4 (APOE4) variant is the single greatest genetic risk factor for sporadic Alzheimer's disease (sAD).
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Apolipoprotein E (ApoE) is an important lipid carrier in both the periphery and the brain.
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39/100
Alzheimer's disease (AD) is a progressive degenerative neurological disorder affecting nearly one in nine elderly people in the United States.
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Age and apolipoprotein E (ApoE) are the mightiest risk factors for dementia and cardiovascular diseases, but the underlying mechanisms remain unclear.
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Population-attributable risk models estimate that up to one-third of Alzheimer's disease (AD) cases may be preventable through risk factor modification.
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Accumulation and aggregation of amyloid-β (Aβ) in the brain is an initiating step in the pathogenesis of Alzheimer's disease (AD).
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Elevated reactive oxygen species (ROS) induce the formation of lipids in neurons that are transferred to glia, where they form lipid droplets (LDs).
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Recent studies have supported a role for the proteolytic cleavage of apolipoprotein E4 (APOE4) as a potential mechanism for the enhanced dementia risk associated with Alzheimer's disease.
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Apolipoprotein E4 (ApoE4) is a major genetic risk factor for sporadic or late onset Alzheimer's disease (AD).
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The apolipoprotein E (apoE) gene has been implicated in various conditions, most notably Alzheimer's disease and coronary artery disease.
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Human apolipoprotein E (ApoE) apolipoprotein is primarily expressed in three isoforms (ApoE2, ApoE3, and ApoE4) that differ only by two residues.
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As the population ages, neurodegenerative diseases such as Alzheimer's disease (AD) are becoming a significant burden on patients, their families, and health-care systems.
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In a cell free assay, ADAM10 activity was found to be significantly lower in apoE4 samples compared to apoE2. 7WCHO cells over expressing wild type AβPP exposed to apoE4 demonstrated reduced formation of sAβPPα compared to other apoE isoforms.
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Apolipoprotein E (apoE) is associated with lipoproteins in the cerebrospinal fluid (CSF).
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The APOE gene is one of currently only two genes that have consistently been associated with longevity.
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Apolipoprotein (apo) E was initially described as a lipid transport protein and major ligand for low density lipoprotein (LDL) receptors with a role in cholesterol metabolism and cardiovascular disease.
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The Alzheimer's disease risk gene apolipoprotein E epsilon 4 (APOE ε4) is associated with increased cerebral amyloid.
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In this study, we show that apoE lipoprotein particles from conditioned media of immortalized astrocytes isolated from human APOE-targeted replacement (TR) mice significantly suppress cellular Aβ42 and Aβ40 uptake through cell surface HSPG.
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Higher HOMA-IR was associated with higher sAβPPβ and Aβ42 .
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Apolipoprotein E receptor 2 (ApoER2) is an apolipoprotein E receptor involved in long-term potentiation, learning, and memory.
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The blood–brain barrier (BBB) limits the entry of neurotoxic blood-derived products and cells into the brain that is required for normal neuronal functioning and information processing.
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Dysregulation of amyloid-β (Aβ) metabolism is critical for Alzheimer's disease (AD) pathogenesis.
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41/100
SMC ε4+ showed greater amyloid deposition than SMC ε4-, but no hypometabolism or medial temporal lobe (MTL) atrophy.
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Our data indicated that the levels of triglyceride, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apolipoprotein A-I (ApoA-I), ApoB, ApoE, lipoprotein (a) (Lp(a)) of mutant genotypes in ApoE c.61G > A and c.761T > A genetic variants were different from those subjects with wild genotype in HD patients and healthy controls.
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Chronic glial activation and neuroinflammation induced by the amyloid‐β peptide (Aβ) contribute to Alzheimer's disease ( AD ) pathology.
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Cholesterol is an essential component for neuronal physiology not only during development stage but also in the adult life.
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The objective of this meta-analysis was to determine the association of the apolipoprotein E ( ApoE ) gene with exceptional longevity (EL) ( i.e ., reaching 100+ years) by identifying possible unequal distribution of alleles/genotypes in the common variants ε2, ε3, and ε4 among centenarians and younger population.
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The TT genotype of rs688 in the LDLR gene was not found to be associated with elevated levels of total cholesterol or LDL-C.
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Apolipoprotein E type 4 allele (ApoE∊4) is known as a risk gene for the late-onset Alzheimer’s disease, and the relationship between ApoE∊4 and cognitive function of the elderly people has drawn the attention of the scientists.
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Growing evidence indicates that apolipoprotein E (ApoE) is one of the most important candidate genes for influencing the development of hemodialysis (HD).
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48/100
The mean age was 51 ± 12 years. Forty-two of the patients had OSAS.
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Human apolipoprotein E (APOE) exists in three isoforms ɛ2, ɛ3, and ɛ4, of which APOE4 is the main genetic risk factor of Alzheimer's disease (AD).
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Brain pathology of Alzheimer's diseases (AD) and the genetics of autosomal dominant familial AD have been the "lamp posts" under which the AD field has been looking for therapeutic targets.
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36/100
Apolipoprotein (apo) E is a multifunctional protein with central roles in lipid metabolism, neurobiology, and neurodegenerative diseases.
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Beta-amyloid accumulation in brain is a driving force for Alzheimer's disease pathogenesis.
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Humans have three major apolipoprotein E (ApoE) alleles (APOE; ε2, ε3 and ε4) that produce three ApoE protein isoforms.
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36/100
The discovery that the apolipoprotein E (apoE) ε4 allele is genetically linked to both sporadic and familial late-onset Alzheimer's disease (AD) raises the possibility that a dysfunction of the lipid transport system could seriously affect lipid homeostasis in the brain of AD subjects.
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It has been estimated that Alzheimer's disease (AD), the most common form of dementia, will affect approximately 81 million individuals by 2040.
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Apolipoprotein E (ApoE) is an abundant plasma protein that interacts with low density lipoprotein receptors and other proteins, participating in the transport of cholesterol and lipids.
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Alzheimer's disease (AD) is characterized by the accumulation and deposition of amyloid-beta (Aβ) peptides in the brain.
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Among the three human apolipoprotein E (apoE) isoforms, apoE4 increases the risk of Alzheimer's disease (AD).
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The mean coverage of the amino acid sequence of full-length ApoE was 91.6% in the protein resequence.
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Late-onset Alzheimer's disease (LOAD) risk is strongly influenced by genetic factors such as the presence of the apolipoprotein E ε4 allele (referred to here as APOE4), as well as non-genetic determinants including ageing.
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Apolipoprotein E gene (APOE) alleles may shift the onset of Alzheimer's disease (AD) through apoE protein isoforms changing the probability of amyloid-β (Aβ) accumulation.
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ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and has been detected in macrophages, microglia, and neurons.
From across this tag
9 of the 268 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
- Amelioration of Tau and ApoE4-linked glial lipid accumulation and neurodegeneration with an LXR agonist
- APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics
- Reduced binding of apoE4 to complement factor H promotes amyloid-β oligomerization and neuroinflammation
- APOE2 mitigates disease-related phenotypes in an isogenic hiPSC-based model of Alzheimer's disease
- Apolipoprotein E in animal models of CNS injury and in Alzheimer's disease
- APOE4-related differences in cortical thickness are modulated by sex in middle age
- A Quarter Century of APOE and Alzheimer's Disease: Progress to Date and the Path Forward
- ApoE4 decreases spine density and dendritic complexity in cortical neurons in vivo
- APOE2: protective mechanism and therapeutic implications for Alzheimer's disease