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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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Alzheimer's disease (AD) is the most common cause of dementia, yet there is no cure or diagnostics available prior to the onset of clinical symptoms.
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Alzheimer's disease (AD) is the foremost type of dementia that afflicts considerable morbidity and mortality in aged population.
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Alzheimer disease (AD) is a heterogeneous disease with many genes are associated with AD risk.
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Identifying biomarkers associated with Alzheimer's disease (AD) progression may enable patient enrichment and improve clinical trial designs.
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The evident genetic, pathological, and clinical heterogeneity of Alzheimer's disease (AD) poses challenges for traditional drug development.
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An arginine-rich apolipoprotein was discovered 50 years ago and became known as apolipoprotein E (ApoE) 10 years later.
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Strikingly gene-expression, network-based analysis and cell type deconvolution approaches revealed a consistent immune signature in the brain and blood of female AD patients that was absent in males.
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These results from the largest longitudinal cohort registry of patients with CAA-ri support the transient and potentially relapsing inflammatory nature of the clinical-radiologic acute manifestations of the disease and the effectiveness of slow oral tapering off after IV corticosteroid pulse therapy in preventing recurrences.
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Human genetic association studies point to immune response and lipid metabolism, in addition to amyloid-beta (Aβ) and tau, as major pathways in Alzheimer's disease (AD) etiology.
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Though apolipoprotein E ε4 (APOE ε4) is a major genetic risk factor for late-onset Alzheimer's disease, its association with depression remains controversial.
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Late-onset Alzheimer's disease is a prevalent age-related polygenic disease that accounts for 50-70% of dementia cases.
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Mechanisms underlying the protective effect of apolipoprotein E (APOE) ε2 against Alzheimer disease (AD) are not well understood.
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Here, we report that the acute exposure of primary cortical neurons or synaptoneurosomes to APOE4 leads to a significant decrease in global protein synthesis.
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43/100
Here, we found a close association of the metabolic reconfiguration of microglia with increased hippocampal glucose uptake on [ 18 F]fluorodeoxyglucose (FDG) PET.
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Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder that involves dysregulation of many cellular and molecular processes.
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APOE4 is a strong genetic risk factor for Alzheimer's disease and Dementia with Lewy bodies; however, how its expression impacts pathogenic pathways in a human-relevant system is not clear.
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The ε4 allele of APOE-encoding apolipoprotein (ApoE) is one of the strongest genetic risk factors for Alzheimer's disease (AD).
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These findings suggest that DPP-4i use is associated with low amyloid burden and favorable long-term cognitive outcome in diabetic patients with ADCI.
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We evaluated whether insomnia symptom severity was associated with cognitive function, and whether this relationship was modified by biomarkers associated with Alzheimer's disease risk.
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These results indicate lipid droplet accumulation occurs in human DAM xMGs in AD, but is reduced in TREM2-R47H DAM xMGs, as it occurs secondary to TREM2-mediated changes in plaque proximity and reactivity.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder with obscure pathogenesis and no disease-modifying therapy to date.
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Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear.
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Amyloid PET and sleep duration information was acquired on 4425 cognitively unimpaired participants (mean [SD] age, 71.3 [4.7] years; 2628 [59.4%] female; 1509 [34.1%] tested Aβ positive).
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Age-related macular degeneration (AMD) is a multifactorial retinal disorder that is a major global cause of severe visual impairment.
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APOE and Trem2 are major genetic risk factors for Alzheimer's disease (AD), but how they affect microglia response to Aβ remains unclear.
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Apolipoprotein E (APOE) ε4 is the single most important genetic risk factor for cognitive impairment and Alzheimer disease (AD), while lifestyle factors such as smoking, drinking, diet, and physical activity also have impact on cognition.
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Since the identification of the apolipoprotein E (apoE) *ε4 allele as a major genetic risk factor for late-onset Alzheimer's disease, significant efforts have been aimed at elucidating how apoE4 expression confers greater brain amyloid-β (Aβ) burden, earlier disease onset and worse clinical outcomes compared to apoE2 and apoE3.
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Neither fibrillar nor nonfibrillar Aβ content alone sufficed to explain the Aβ PET findings in either AD model.
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63/100
The plasma proteomic changes that precede the onset of dementia could yield insights into disease biology and highlight new biomarkers and avenues for intervention.
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Alzheimer's disease (AD) is an incurable neurodegenerative disease currently affecting 1.75% of the US population, with projected growth to 3.46% by 2050.
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Alzheimer's disease (AD) is the most common form of dementia, currently affecting 35 million people worldwide.
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61/100
Genome-wide association studies (GWAS) have identified polymorphism in the Apolipoprotein E gene (APOE) to be the most prominent risk factor for Alzheimer's disease (AD).
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The apolipoprotein E (APOE) gene is the strongest genetic risk factor for Alzheimer's disease and directly influences tauopathy and tau-mediated neurodegeneration.
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Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD).
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The extracellular deposition of β-amyloid (Aβ) is one of the major characteristics in Alzheimer´s disease (AD).
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Emerging evidence indicates that impaired mitophagy-mediated clearance of defective mitochondria is a critical event in Alzheimer's disease (AD) pathogenesis.
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43/100
These data demonstrate the neuroprotective effects of systemic administration of stem cell-derived EVs for remediation of behavioral and molecular AD neuropathologies.
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Alzheimer's disease (AD) is associated with abnormal tau and amyloid-β accumulation in the brain, leading to neurofibrillary tangles, neuropil threads and extracellular amyloid-β plaques.
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Alzheimer disease (AD) is the most prevalent neurodegenerative disorder leading to dementia in the elderly.
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The gut microbiota (GM) represents a diverse and dynamic population of microorganisms and about 100 trillion symbiotic microbial cells that dwell in the gastrointestinal tract.
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Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown.
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Neuroinflammation is a common feature in neurodegenerative diseases, modulated by the Alzheimer's disease risk factor, apolipoprotein E (APOE).
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The ε4 allele of the apolipoprotein E ( APOE ) gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and greatly influences the development of amyloid-β (Aβ) pathology.
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We analyzed data from 462 ADNI participants without dementia who underwent Aβ ([ 18 F]florbetapir or [ 18 F]florbetaben) and tau ([ 18 F]flortaucipir) PET, structural MRI, and cognitive testing.
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AD patients with ELA expressed significantly greater levels of APOE than ALA APOE ε4 carriers.
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Genetic and genome-wide association studies suggest a central role for microglia in Alzheimer's disease (AD).
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Congo Red (CR) has been used for its binding affinity to amyloid fibrils for the better part of a century.
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It has been well established that the TMEM106B gene rs1990622 variant was a frontotemporal dementia (FTD) risk factor.
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Intimate metabolic host-microbiome crosstalk regulates immune, metabolic, and neuronal response in health and disease, yet remains untapped for biomarkers or intervention for disease.
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The hallmarks of Alzheimer's disease (AD) pathology include senile plaques accumulation and neurofibrillary tangles, which is thought to underlie synaptic failure.
From across this tag
10 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 10. The same 10 appear here every time.
- Differential and substrate-specific inhibition of γ-secretase by the C-terminal region of ApoE2, ApoE3, and ApoE4
- Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction
- Complete genomic screen in late-onset familial Alzheimer disease. Evidence for a new locus on chromosome 12
- The Role of Apolipoprotein E in Alzheimer's Disease
- Powerful beneficial effects of macrophage colony-stimulating factor on beta-amyloid deposition and cognitive impairment in Alzheimer's disease
- Role of the toll-like receptor 4 in neuroinflammation in Alzheimer's disease
- Fine-mapping HLA-II haplotypes in Alzheimer's disease and healthy longevity reveals distinct associations with microglial HLA-II load and neuropathology
- Apolipoprotein E epsilon4 count affects age at onset of Alzheimer disease, but not lifetime susceptibility: The Cache County Study
- Multi-ancestry genome-wide meta-analysis of 56,241 individuals identifies known and novel cross-population and ancestry-specific associations as novel risk loci for Alzheimer's disease
- Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomers