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apolipoprotein
1,613 studies tagged apolipoprotein, dated 1982-09-01 to 2026-10-27. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
1,613 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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We show that m 6 A modification displays temporal and spatial dynamics during neurodevelopment and aging.
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74/100
The APOE ε4 allele remains the strongest genetic risk factor for sporadic Alzheimer's disease and the APOE ε2 allele the strongest genetic protective factor after multiple large scale genome-wide association studies and genome-wide association meta-analyses.
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In addition, several loci associated with rare variants, including a genome-wide significant intergenic locus near IGF1R at 15q26 (P = 1.7 × 10-9) and 6 additional loci with suggestive significance (P ≤ 5 × 10-7) such as API5 at 11p12 (P = 8.8 × 10-8) and RBFOX1 at 16p13 (P = 5.4 × 10-7) were identified.
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These findings suggest that OCT can detect functional and morphologic changes in the retina of carriers of familial Alzheimer disease who are cognitively unimpaired several years before clinical onset, suggesting that OCT findings and retinal vascular parameters may be biomarkers prior to the onset of cognitive decline.
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For years, it has been reported that Alzheimer's disease (AD) is the most common cause of dementia.
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Clinical phenotypes are associated with differential patterns of tau but not amyloid pathology.
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Variations in many genes linked to sporadic Alzheimer's disease (AD) show abundant expression in microglia, but relationships among these genes remain largely elusive.
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Mechanisms underlying the protective effect of apolipoprotein E ( APOE ) ε2 against Alzheimer’s disease (AD) are not well understood.
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Amyloid-β (Aβ) deposits are a relatively late consequence of Aβ aggregation in Alzheimer's disease.
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Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD).
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Apolipoprotein E (ApoE) is of great interest due to its role as a cholesterol/lipid transporter in the central nervous system (CNS) and as the most influential genetic risk factor for Alzheimer disease (AD).
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Investigations of apolipoprotein E (APOE) gene, the major genetic risk modifier for Alzheimer's disease (AD), have yielded significant insights into the pathogenic mechanism.
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As predicted, we observed a differential impact of CBE status on cognition as a function of APOE ε4 status, in which CBE ε4 carriers displayed significantly worse neuropsychological performance, specifically in the domain of memory.
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APOE4 is the strongest genetic risk factor associated with late-onset Alzheimer's disease (AD).
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50/100
Gut microbiota represents a diverse and dynamic population of microorganisms harboring the gastrointestinal tract, which influences the host health and disease.
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Combining human cohort data (over 24,000 people) with mouse models, this study found that carrying the APOE2 gene variant is linked to a longer lifespan, and that this benefit holds even when accounting for Alzheimer's diagnosis and brain pathology.
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Over 35% of the adult US population is obese.
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The largest cohort, the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease Study (n = 3154), was the PET screening cohort used for a secondary prevention trial designed to slow cognitive decline associated with brain amyloidosis.
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Dementia is a rapidly rising global health crisis that silently disables families and ends lives and livelihoods around the world.
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However, the clinical presentation, associated factors, frequency in community-based cohorts, genetic characteristics, and cognitive trajectories associated with the quadruple misfolded proteins phenotype are not well understood.
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Alzheimer's disease (AD) is the most prevalent form of late-onset dementia.
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Microglia-specific genetic variants are enriched in several neurodegenerative diseases, including Alzheimer's disease (AD), implicating a central role for alterations of the innate immune system in the disease etiology.
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Apolipoprotein E (APOE) is the major cholesterol carrier in the brain, affecting various normal cellular processes including neuronal growth, repair and remodeling of membranes, synaptogenesis, clearance and degradation of amyloid β (Aβ) and neuroinflammation.
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Obesity is a multifactorial disease in which environmental conditions and several genes play an important role in the development of this disease.
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The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD).
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In 1907, Alois Alzheimer observed, as he quoted, development of "numerous fibers" and "adipose saccules" in the brain of his diseased patient Auguste Deter.
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Microglia activation is the brain's major immune response to amyloid plaques in Alzheimer's disease (AD).
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Genetic and epidemiological studies have found that variations in the amyloid precursor protein (APP) and the apoliopoprotein E (APOE) genes represent major modifiers of the progressive neurodegeneration in Alzheimer's disease (AD).
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Low serum albumin may increase the risk of AD dementia by elevating amyloid accumulation.
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'Triggering receptor expressed on myeloid cells 2' (TREM2) gene is involved in Alzheimer's disease (AD) and TREM2 mRNA expression is known to be increased in the peripheral blood cells of AD patients.
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Clinical trials focusing on therapeutic candidates that modify β-amyloid (Aβ) have repeatedly failed to treat Alzheimer's disease (AD), suggesting that Aβ may not be the optimal target for treating AD.
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Apolipoprotein E (APOE) has been shown to influence amyloid-β (Aβ) clearance from the brain in an isoform-specific manner.
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The genotype KL-VSHET+ is associated with reduced AD risk and Aβ burden in individuals who are aged 60 to 80 years, cognitively normal, and carrying APOE4.
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Globally, 50 million people live with dementia, with Alzheimer disease (AD) being responsible for two-thirds of the total cases.
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A new study suggests that the leading genetic risk factor for Alzheimer's disease, apolipoprotein E4 (APOE4), is linked to blood-brain barrier breakdown and subsequent cognitive decline.
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The APOE gene alleles modify human aging and the response to the diet at many levels with diverse pleotropic effects from gut to brain.
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ApoE isoforms influence mitochondrial structure and function, which likely leads to alteration in oxidative stress, synapses, and cognitive function.
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Since the world population is ageing, dementia is going to be a growing concern.
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CSF levels of apoE2, apoE3, and apoE4 were significantly higher (all nominal P < 10 × 10-5 , false discovery rate < 0.001) and those of tumor necrosis factor-α (TNF-α) were significantly lower (nominal P = 1.39 × 10-6 , false discovery rate < 0.001) in APOE-ε4 carriers than in noncarriers.
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The pathogenesis of Alzheimer's disease (AD) and the commonest cause of dementia in the elderly remain incompletely understood.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease that causes chronic cognitive dysfunction.
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39/100
Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disease, currently affecting over 5 million Americans with projections expected to rise as the population ages.
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Vascular contributions to dementia and Alzheimer's disease are increasingly recognized 1-6 .
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Our proof-of-concept study is the first to show that microstructural and macrostructural changes can reflect underlying neuroinflammatory mechanisms in early stages of Alzheimer disease (AD).
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It is increasingly accepted that early cognitive impairment in Alzheimer's disease results in considerable part from synaptic dysfunction caused by the accumulation of a range of oligomeric assemblies of amyloid β-protein (Aβ).
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Type I interferon (IFN) is a key cytokine that curbs viral infection and cell malignancy.
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Evidence suggests interplay among the three major risk factors for Alzheimer's disease (AD): age, APOE genotype, and sex.
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Peroxisome proliferator activated receptor alpha (PPAR-α) belongs to the family of ligand-regulated nuclear receptors (PPARs).
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Various brain injuries lead to the activation of adult neural stem/progenitor cells in the mammalian hippocampus.
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Intracranial atherosclerotic disease (ICAD) is an important cause of stroke and has also been recently identified as an important risk factor for all-cause dementia, but the mechanism of its association with cognitive performance is not fully understood.
From across this tag
9 of the 1,611 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.
- Whole-genome sequencing reveals new Alzheimer's disease-associated rare variants in loci related to synaptic function and neuronal development
- Association of Platelet Aggregation With Markers of Alzheimer Disease Pathology in Middle-Aged Participants of the Framingham Heart Study
- A dual role for apolipoprotein e in neuroinflammation: anti- and pro-inflammatory activity
- EEG alterations in non-demented individuals related to apolipoprotein E genotype and to risk of Alzheimer disease
- P-glycoprotein deficiency at the blood-brain barrier increases amyloid-beta deposition in an Alzheimer disease mouse model
- Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation
- Changes in cerebral blood volume and amyloid pathology in aged Alzheimer APP/PS1 mice on a docosahexaenoic acid (DHA) diet or cholesterol enriched Typical Western Diet (TWD)
- Shorter telomeres are associated with mortality in those with APOE epsilon4 and dementia
- Plasma amyloid levels and the risk of AD in normal subjects in the Cardiovascular Health Study