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apoe2
266 studies tagged apoe2, 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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Alzheimer's disease (AD) is the most common cause of late-life dementia characterized by progressive neurodegeneration and brain deposition of amyloid-β (Aβ) and phosphorylated tau.
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Isogenic BMEC-like cells with different APOE genotypes had similar trans-endothelial electrical resistance, tight junction integrity and efflux transporter gene expression.
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Alzheimer's disease (AD) is an incurable and progressive neurodegenerative disease with increasing prevalence worldwide.
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Apolipoprotein E4 (ApoE4) plays an important role responding to monomeric C-reactive protein (mCRP) via binding to CD31 leading to cerebrovascular damage and Alzheimer's disease (AD).
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Apolipoprotein E (APOE) ε4, the strongest genetic risk for late-onset Alzheimer's disease (AD), confers greater risk in females than males.
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The strongest genetic risk factor for late-onset Alzheimer's disease (AD) is allelic variation of the APOE gene, with the following risk structure: ε4 > ε3 > ε2.
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Human apolipoprotein E (ApoE) was first identified as a polymorphic gene in the 1970s; however, the genetic association of ApoE genotypes with late-onset sporadic Alzheimer's disease (sAD) was only discovered 20 years later.
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The study population consisted of 194 patients (123 AD and 71 non-AD).
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The apolipoprotein E4 (APOE4) allele represents the major genetic risk factor for Alzheimer's disease (AD).
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Apolipoprotein E (APOE) is a major cholesterol carrier responsible for lipid transport and injury repair in the brain.
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The pathway analysis of six major cell types revealed a strong association between APOE2 and cellular stress and energy metabolism, particularly in excitatory and inhibitory neurons, which was found to be more pronounced in the presence of beta-amyloid (Aβ).
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The targeting of amyloid-beta (Aβ) plaques therapeutically as one of the primary causes of Alzheimer's disease (AD) dementia has been an ongoing effort spanning decades.
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We identified sex differences for several classes of metabolites, such as glycerophospholipids, sphingolipids, and amino acids.
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Omega-3 (n-3) polyunsaturated fatty acids (PUFAs), such as docosahexaenoic acid (DHA), have important roles in human nutrition and brain health by promoting neuronal functions, maintaining inflammatory homeostasis, and providing structural integrity.
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Several genetic risk factors for Alzheimer's disease implicate genes involved in lipid metabolism and many of these lipid genes are highly expressed in glial cells 1 .
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Increasing evidence suggests that the calcium-binding and proinflammatory protein S100A9 is an important player in neuroinflammation-mediated Alzheimer's disease (AD).
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In this narrative review, we delved into the intricate interplay between Apolipoprotein E (APOE) alleles (typically associated with Alzheimer's disease-AD) and alpha-synucleinopathies (aS-pathies), involving Parkinson's disease (PD), Parkinson's disease dementia (PDD), dementia with Lewy bodies (DLB), and multiple-system atrophy (MSA).
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The pleiotropic nature of the apolipoprotein E (APOE) gene is associated with complex diseases in different populations.
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Alzheimer's disease (AD) is a neurodegenerative disease with a complex etiology influenced by confounding factors such as genetic polymorphisms, age, sex, and race.
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Among CN, APOE4 carriers showed lower entorhinal cortex neurite density than non-carriers, whereas APOE2 carriers showed lower cingulum neurite density than non-carriers.
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43/100
The impact of apolipoprotein E (ApoE) isoforms on sporadic Alzheimer's disease has long been studied; however, the influences of apolipoprotein E gene (APOE) on healthy and pathological human brains are not fully understood.
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Apolipoprotein E (APOE) is the single greatest genetic risk factor for late onset Alzheimer's disease (AD).
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Human apolipoprotein E (APOE) is the greatest determinant of genetic risk for memory deficits and Alzheimer's disease (AD).
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Apolipoprotein E (APOE) is a strong genetic risk factor for late-onset Alzheimer's disease (LOAD).
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Apolipoprotein E (APOE) traffics lipids in the central nervous system.
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41/100
APOE germline variants impact melanoma progression through disparate mechanisms, such as the protein synthesis-promoting function of the APOE2 variant, indicating that germline genetic variants are causal contributors to metastatic outcomes.
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β amyloid protein (Aβ)1-42 level from the APOE ε4 carrier group was significantly lower than that from the non-carrier group (p = 0.023), which was associated with worse cognitive function.
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Although aging and apolipoprotein E (APOE) ε4 allele have been documented as two major risk factors for late-onset Alzheimer's disease (LOAD), their interaction and potential underlying mechanisms remain unelucidated.
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Obesity was associated with cognitive decline in early elderly cognitively normal individuals without APOE4, especially those with APOE2.
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41/100
Triggering receptor expressed on myeloid cells 2 (TREM2) is a membrane receptor on myeloid cells and plays an important role in the body's immune defense.
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41/100
The Apolipoprotein E ε4 (ApoE ε4) allele, encoding ApoE4, is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD).
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The inheritance of Apolipoprotein E4 (APOEε4) brings the highest genetic risk of Alzheimer's disease (AD), arguably the highest genetic risk in human pathology.
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The APOE4 variant of apolipoprotein E (apoE) is the most prevalent genetic risk allele associated with late-onset Alzheimer's disease (AD).
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Apolipoprotein E (ApoE)'s ϵ4 alle is the most important genetic risk factor for late onset Alzheimer's Disease (AD).
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The apolipoprotein E gene (APOE) confers the greatest genetic risk factor for Alzheimer's disease (AD), wherein the ε4 allele confers an elevated risk compared with the ε3 allele.
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Aberrant low γ-secretase activity is associated with most of the presenilin mutations that underlie familial Alzheimer's disease (fAD).
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Vascular risk significantly predicted cerebral amyloid burden in Alzheimer's Disease Neuroimaging Initiative but not in the UCD-ADRC cohort.
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41/100
The ε4-allele variant of apolipoprotein E (ApoE4) is the strongest genetic risk factor for Alzheimer's disease, although it only differs from its neutral counterpart ApoE3 by a single amino acid substitution.
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Apolipoprotein E4 (ApoE4) is the most recognized genetic risk factor for late-onset Alzheimer's disease (LOAD), whereas ApoE2 reduces the risk for LOAD.
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We found that TDP-43 overexpression induced motor function deficits, neuronal loss, and gliosis in the motor cortex, especially in APOE2 mice, with much milder or absent effects in APOE3, APOE4, or Apoe-KO mice.
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Apolipoprotein E (ApoE) is a multifunctional protein involved in lipid transport and lipoprotein metabolism, mediating lipid distribution/redistribution in tissues and cells.
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APOE4 is the strongest genetic risk factor for Alzheimer's disease 1-3 .
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Apolipoprotein E (ApoE) is a multifaceted secreted molecule synthesized in the CNS by astrocytes and microglia, and in the periphery largely by the liver.
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ApoE is the major lipid and cholesterol carrier in the CNS.
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Clinical outcomes of severe acute respiratory syndrome 2 (SARS-CoV-2) infection are highly heterogeneous, ranging from asymptomatic infection to lethal coronavirus disease 2019 (COVID-19).
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A preponderance of evidence obtained from genetically modified mice and human population studies reveals the association of apolipoprotein E (apoE) deficiency and polymorphisms with pathogenesis of numerous chronic diseases, including atherosclerosis, obesity/diabetes, and Alzheimer's disease.
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48/100
Apolipoprotein E (APOE) plays a pivotal role in lipid including cholesterol metabolism.
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The APOE gene encoding the Apolipoprotein E protein is the single most significant genetic risk factor for late-onset Alzheimer's disease.
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The impact of apolipoprotein E ε4 (APOE4), the strongest genetic risk factor for Alzheimer's disease (AD), on human brain cellular function remains unclear.
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Alzheimer's disease (AD) is the most common type of dementia.
From across this tag
9 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 9. The same 9 appear here every time.
- ApoE4 and Psychosis in Neurodegenerative and Non-Neurodegenerative Disease: A Scoping Review
- Apolipoprotein E isoforms differentially regulate matrix metallopeptidase 9 function in Alzheimer's disease
- Apolipoprotein E variation at the sequence haplotype level: implications for the origin and maintenance of a major human polymorphism
- ApoE2, ApoE3, and ApoE4 Differentially Stimulate APP Transcription and Aβ Secretion
- APOE4 Causes Widespread Molecular and Cellular Alterations Associated with Alzheimer's Disease Phenotypes in Human iPSC-Derived Brain Cell Types
- APP-Induced Patterned Neurodegeneration Is Exacerbated by APOE4 in Caenorhabditis elegans
- APOE ε4: the most prevalent yet understudied risk factor for Alzheimer's disease
- Multimodal mediators connecting APOE4 to dementia
- Functional characterization of apolipoprotein E isoforms overexpressed in Escherichia coli