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apolipoprotein
1,612 studies tagged apolipoprotein, dated 1982-09-01 to 2026-10-27. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
1,612 studies carry this tag.
Date range
1982 to 2026
Top journals
- Neurology 93
- The Journal of biological chemistry 68
- Proceedings of the National Academy of Sciences of the United States of America 52
- Archives of neurology 43
- Neurobiology of aging 38
457 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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Blood-based biomarkers for Alzheimer's disease (AD) pathology have been investigated intensively as markers for AD-related neurodegeneration.
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However, postmortem investigations indicate that the AD-typical progressive amnestic syndrome may also result from predominantly limbic non-AD neuropathology such as TDP-43 proteinopathy and argyrophilic grain disease.
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We observed differential cellular effects on β-amyloid, pTau217 and cognitive measures.
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Alzheimer?s disease (AD) is a neurodegenerative disorder with a strong genetic component.
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• Longitudinal imaging-genetics study of hippocampal atrophy trajectories over 5 years in ADNI. • APOE -ε4 carriership and ApoE CSF proteomic quantitative trait loci are key genetic drivers of accelerated hippocampal atrophy in amyloid-positive MCI. • Genetic effects are stage-specific, with strongest associations during the prodromal phase of AD. • Sex differences in atrophy rates are observed, but do not significantly alter genetic influences. • Findings support the utility of APOE and functional genetic markers as stratification tools for early neurodegeneration in AD.
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Cerebral small vessel disease can manifest as vascular dementia, typically associated with vascular risk factors or cerebral amyloid angiopathy, and more rarely associated with hereditary conditions.
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Alzheimer's disease (AD), the most common form of dementia, is marked by cognitive decline and amyloid-beta (Aβ) plaque deposition in the brain.
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The rising global prevalence of Alzheimer's disease (AD) and mild cognitive impairment (MCI) underscores the urgent need to elucidate their underlying pathogenic mechanisms.
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• EEG microstate analyses were performed in a cohort of autosomal dominant AD. • Coverage of class C decreased in symptomatic mutation carriers • Coverage of class D decreased in presymptomatic and symptomatic mutation carriers. • Coverage of class E increased in presymptomatic and symptomatic mutation carriers. • The findings may support presymptomatic changes in resting-state neuronal networks.
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APOE ε4 is associated with accelerated progression of AD pathology.
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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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Alzheimer's disease (AD) is the most common neurodegenerative dementia with multi-layered complexity in its molecular etiology.
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The role of microglia in the amyloid cascade of Alzheimer's disease (AD) is debated due to conflicting findings.
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We observed a relationship between residence in a more disadvantaged neighborhood (higher ADI) and lower rates of amyloid positivity.
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We observed a relationship between residence in a more disadvantaged neighborhood (higher ADI) and lower rates of amyloid positivity.
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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.
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Gene therapy to treat hereditary disorders conventionally delivers the normal allele to compensate for loss-of-function mutations.
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Quinoa is an ancient Andean crop with a significant interest due to its nutritional and health benefits.
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MR analysis suggested a causal relationship between decreased blood-derived mtDNA-CN and increased risk of AD (OR = 0.68; P = 0.013).
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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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This study highlighted that the AD-causal MD genes could be regulated by epigenetic changes and interact with inflammatory cytokines, providing evidence for AD prevention and intervention.
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Alzheimer's disease (AD) is an incurable and progressive neurodegenerative disease with increasing prevalence worldwide.
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The strongest risk factors for late-onset sporadic Alzheimer's disease (AD) include the ε4 allele of apolipoprotein E (APOE), the R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2), and female sex.
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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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61/100
Impaired cerebral glucose metabolism is a pathologic feature of Alzheimer's disease (AD), with recent proteomic studies highlighting disrupted glial metabolism in AD.
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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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A summary measure of γ-secretase activity (γ-secretase composite [GSC]) was calculated for each variant and compared with clinical history-derived AAO using correlation analyses.
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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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Alzheimer's disease currently has no cure and is usually detected too late for interventions to be effective.
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APP gene dosage is strongly associated with Alzheimer's disease (AD) pathogenesis.
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Isolated forebrain synaptosomes, rather than total homogenates, from atg7 iKO mice demonstrated accumulation of synaptic proteins, suggesting that the synapse might be a vulnerable site for protein homeostasis disruption.
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Eighteen years after it was published, Nature formally retracted the landmark 2006 paper that had proposed a specific amyloid protein (Aβ*56) as a cause of memory loss in mice, citing evidence of image manipulation, including splicing, duplication, and use of an image-editing 'eraser' tool.
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Clinical data supported a delayed onset of cognitive impairment in persons who were heterozygous for the APOE3 Ch variant in a kindred with a high prevalence of autosomal dominant Alzheimer's disease.
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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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Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed.
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This study aimed to evaluate the impact of APOE4 homozygosity on Alzheimer's disease (AD) by examining its clinical, pathological and biomarker changes to see whether APOE4 homozygotes constitute a distinct, genetically determined form of AD.
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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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Analyzing postmortem brain pathology from over 3,200 people plus biomarker data from more than 10,000 more, researchers found that people who inherit two copies of the APOE4 gene variant (about 2-3% of the population) develop Alzheimer's brain changes almost universally and on a predictable timeline starting around age 55, much like known single-gene forms of Alzheimer's. The authors argue this makes APOE4 homozygosity itself a genetic form of Alzheimer's disease rather than just a risk factor.
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We identified sex differences for several classes of metabolites, such as glycerophospholipids, sphingolipids, and amino acids.
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Research evidence indicating common metabolic mechanisms through which type 2 diabetes mellitus (T2DM) increases risk of late-onset Alzheimer's dementia (LOAD) has accumulated over recent decades.
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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.
From across this tag
8 of the 1,610 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.
- Encephalopathy with idiopathic hyperammonaemia and Alzheimer type II astrocytes in equidae
- Spontaneous ARIA-like Events in Cerebral Amyloid Angiopathy-Related Inflammation: A Multicenter Prospective Longitudinal Cohort Study
- Brain oligomeric β-amyloid but not total amyloid plaque burden correlates with neuronal loss and astrocyte inflammatory response in amyloid precursor protein/tau transgenic mice
- Apolipoprotein E genotype and neurological disease onset in Niemann-Pick disease, type C1
- Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a ‘thrifty’ allele?
- Mesenchymal stem cells enhance autophagy and increase β-amyloid clearance in Alzheimer disease models
- The triggering receptor expressed on myeloid cells 2-apolipoprotein E signaling pathway in diseases
- Dysfunctionally phosphorylated type 1 insulin receptor substrate in neural-derived blood exosomes of preclinical Alzheimer's disease