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apoe4
266 studies tagged apoe4, dated 1993-09-01 to 2026-10-27. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
266 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
168 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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Psychosis is a neuropsychiatric feature found across neurodegenerative conditions including Alzheimer’s disease (AD) and Parkinson’s disease (PD).
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We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints.
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Alzheimer’s disease (AD) affects women more than men, with risk increasing during and after the menopausal transition.
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Plasma APOE4 proteotyping accurately distinguished genotype-defined APOE ε4 carrier status and copy number while demonstrating AD-related associations comparable to DNA genotyping.
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This study analyzed 871 eyes from 439 participants (230 APOE ε4 noncarriers and 209 carriers).
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Cerebral amyloid angiopathy (CAA), characterized by cerebrovascular amyloid deposition, is strongly associated with Alzheimer’s disease, ischemic injury, and lobar hemorrhages.
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In this cohort, APOE ε4 carrier status was related to disease severity at baseline rather than to the rate of cognitive decline over 80 weeks.
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Apolipoprotein E (APOE) genotype is theorised to influence dementia risk partly through effects on blood–brain barrier (BBB) function, but clinical studies examining APOE effects on BBB biomarkers report inconsistent results.
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We identified 27 phenotypes associated with APOE, mainly in neurological and lipid-related traits.
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Previous experimental studies suggested a link between the apolipoprotein E (APOE) gene and epilepsy.
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Cerebrovascular disease is a major but poorly understood feature of Alzheimer's disease (AD).
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Pericytes are critical for maintaining blood-brain barrier (BBB) integrity and have emerged as key contributors to Alzheimer's disease (AD) pathogenesis.
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The apolipoprotein E ε4 (APOE4) allele is the strongest genetic risk factor for developing sporadic Alzheimer’s disease (AD), which accounts for the vast majority of AD cases.
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16/100
Genetic variation in APOE , which encodes a lipid transporter apolipoprotein E (apoE), is the strongest risk factor for late-onset Alzheimer’s disease (AD).
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16/100
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, and its incidence is rising rapidly with population aging.
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The apolipoprotein E ε4 ( APOE ε4) allele is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD), yet its associated protein changes across biofluids, brain regions, and cell types remain incompletely understood.
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This study demonstrated that APOE4 carrier status was associated with lower MoCA-INA scores in this small VaD cohort.
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Apolipoprotein E4 (APOE4) is a major risk factor for Alzheimer’s disease (AD).
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Lipid droplets are dynamic cellular organelles that store neutral lipids and coordinate metabolic and stress-response pathways.
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Anti-amyloid antibodies represent the first disease modifying therapeutics for Alzheimers disease (AD).
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The ratio showed excellent separation across genotypes in our cohort.
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Genome-wide association studies (GWAS) have identified APOE2 allele as linked to exceptional longevity, with carriers exhibiting a reduced risk of Alzheimer's disease (AD).
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Individuals with Alzheimer's disease (AD) are at an increased risk of bone fracture, while osteoporosis in women is one of the earliest predictors of AD.
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Individuals who carry two copies of the apolipoprotein E ε4 ( APOE ε4) allele are at high risk of developing Alzheimer’s disease (AD), yet the effects of APOE ε4 homozygosity on biological pathways related to AD over the lifespan are unknown.
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The APOE4 variant was the strongest genetic risk factor for sporadic Alzheimer's disease (AD).
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Based on the folding energy (ΔΔG) calculations, mutations G165W and L155W were particularly destabilizing in APOE4.
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Sporadic Alzheimer's disease (sAD) is marked by dysregulated lipid metabolism, prominently involving apolipoprotein E (ApoE).
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Apolipoprotein E (ApoE) mediates the bidirectional transport of lipids between cells.
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73/100
In TRIAD, ALZpath p-tau217 (β = 0.45, p = 0.02) and p-tau217+Janssen (β = 0.67, p = 0.002), and in ADNI p-tau217 (β = 0.90, p = 0.002) increased faster in A+E4+.
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Apolipoprotein E (APOE) is the major lipid transport protein in the brain.
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Compared to individuals carrying two copies of the ε4 allele of apolipoprotein E (APOE), ε2 homozygotes have an approximate 99% reduction in late-onset Alzheimer's disease (AD) risk.
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The brain is the most cholesterol-rich organ in the body, and ApoE is the main lipid carrier protein in the brain.
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In the SAA-APP knock-in model of dense-cored Aβ deposits resulting from accumulation of protofibrillar-favoring Aβ42, we observed that crossing in human APOE reduced amyloid burden.
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Cerebrovascular disease is a major but poorly understood feature of Alzheimer's disease (AD).
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We investigated associations between apolipoprotein E (APOE) alleles and motor manifestations in Alzheimer's dementia (AD) capitalizing on National Alzheimer's Coordinating Center data: the baseline evaluations of older adults (≥60 years) with a diagnosis of AD were analyzed.
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ATP Seahorse assay revealed a reduced mitochondrial and glycolytic ATP production in APOE4 iAstrocytes.
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The lipids and proteins that comprise lipid droplets regulate several cellular functions including lipid storage, stress responses, and inflammation.
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ApoE4 levels ascertained by the e4Quant test exhibited clear genotype-dependent stratification.
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Apolipoprotein E (ApoE) variants are central to Alzheimer's disease (AD), Lewy body dementia (LBD) and Niemann-Pick disease type C (NPC).
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The ApoE-ε4 gene is a well-established genetic risk factor for neurodegenerative diseases, such as Alzheimer's disease and multiple sclerosis, which are characterized by axonal demyelination in the central nervous system.
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Alzheimer's disease (AD) is a predominant form of dementia in elderly.
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The apolipoprotein E (APOE) gene is the strongest genetic risk modifier for Alzheimer's disease (AD), with the APOE4 allele increasing risk and APOE2 decreasing it compared with the common APOE3 allele.
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Trisomy of chromosome 21, the cause of Down syndrome (DS), is the most commonly occurring genetic cause of Alzheimer’s disease (AD).
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APOE4-KI mice showed impaired retinal structure, vasculature, function, vision, increased gliosis and neuroinflammation, and downregulation of synaptogenesis.
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Alzheimer's disease (AD), the most common kind of dementia worldwide, is characterized by elevated levels of the amyloid-β (Aβ) peptide and hyperphosphorylated tau protein in the neurons.
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Although APOE ε2 is known to be protective against Alzheimer's disease, it has also been shown to increase risk for hemorrhage with cerebral amyloid angiopathy.
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Apolipoprotein E (ApoE) polymorphisms modify the risk of Alzheimer's disease with ApoE4 strongly increasing and ApoE2 modestly decreasing risk relative to the control ApoE3.
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The major genetic risk factor for Alzheimer's disease (AD), APOE4, accelerates beta-amyloid (Aβ) plaque formation, but whether this is caused by APOE expressed in microglia or astrocytes is debated.
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While apolipoprotein E (APOE) is the strongest genetic modifier for late-onset Alzheimer's disease (LOAD), the molecular mechanisms underlying isoform-dependent risk and the relevance of ApoE-associated lipids remain elusive.
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43/100
Alzheimer's disease (AD) is a complex neurodegenerative disorder influenced by various genetic factors.
From across this tag
8 of the 266 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 8. The same 8 appear here every time.
- ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models
- APOE4 impairs myelination via cholesterol dysregulation in oligodendrocytes
- ABCA1 Is Required for Normal Central Nervous System ApoE Levels and for Lipidation of Astrocyte-secreted apoE
- Dysregulation of cholesterol balance in the brain: contribution to neurodegenerative diseases
- The Glia-Neuron Lactate Shuttle and Elevated ROS Promote Lipid Synthesis in Neurons and Lipid Droplet Accumulation in Glia via APOE/D
- APOE4 derived from astrocytes leads to blood-brain barrier impairment
- Vascular Risk Predicts Plasma Amyloid β 42/40 Through Cerebral Amyloid Burden in Apolipoprotein E ε4 Carriers
- Human apolipoprotein E ɛ4 expression impairs cerebral vascularization and blood-brain barrier function in mice