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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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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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The causes of late onset Alzheimer disease (LOAD) are not known but several recent lines of evidence implicate the adaptive immune system.
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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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Symptomatic DIAD participants who had been treated for ∼ 4 years with anti-Aβ monoclonal antibodies (gantenerumab, n=4 or solanezumab, n=4) were compared with untreated, symptomatic DIAD mutation carriers (n=40) and with age-relevant non-DIAD controls with modest or no plaque pathology (n=18).
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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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Stroke and dementia are leading causes of death and disability worldwide, requiring enhanced preventive strategies.
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Cerebrovascular disease is a major but poorly understood feature of Alzheimer's disease (AD).
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INTRODUCTIONInflammation plays a central role in Alzheimers Disease (AD), with oxylipins, endocannabinoids, and polyunsaturated fatty acids (PUFAs) acting as potent modulators.
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Cellular mechanisms in early Alzheimers disease (AD) remain poorly understood despite generation of extensive observational multiomic data.
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INTRODUCTIONAlzheimers, Lewy body and vascular neuropathology underpin the most common forms of dementia.
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder whose genetic architecture and underlying molecular mechanisms remain incompletely understood, particularly in sporadic disease.
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Structured AbstractO_ST_ABSBackgroundC_ST_ABSThe genetic architecture of Alzheimer disease remains incompletely understood.
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Alzheimers disease and related dementias (ADRD)1 and Parkinsons disease and related disorders (PDRD)2 have substantial genetic contributions, yet the role of rare damaging coding variants remains incompletely characterized at population scale3-6.
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ImportanceAnxiety phenotypes - rumination, global anxiety, and worry (RAW) - are increasingly associated with Alzheimers disease and related dementias (ADRD) risk, yet how anxiety phenotypes relate to coordinated, multi-system biology in the at-risk older adults is unknown.
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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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APOE and PICALM are prominent risk genes for late-onset Alzheimer’s disease (AD).
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 .
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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
BackgroundClonal haematopoiesis (CH), the age-related expansion of mutated blood stem cells, is detectable in around 10% of people in their seventies, rises steeply with age, and is associated with several diseases.
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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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BackgroundAnti-amyloid-{beta} (A{beta}) monoclonal antibodies are disease-modifying treatments for early Alzheimers disease but are associated with amyloid-related imaging abnormalities (ARIA) and intracranial hemorrhage (ICH).
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ResultsThe CNR2 missense variant rs4649124 was associated with increased vascular dementia risk (BH-adjusted P = 0.049) after correction at the 5% false discovery rate (FDR) threshold, with additional associations at the 10% FDR threshold for all-cause dementia risk (BH-adjusted P = 0.051) and lower circulating APP (BH-adjusted P = 0.088) and BDNF (BH-adjusted P = 0.083) levels.
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BackgroundAlzheimers disease (AD) pathology often accumulates years before memory loss, creating a need to identify high-risk individuals presymptomatically.
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Sex differences in Alzheimers disease (AD) genetic effects and regulatory contexts remain incompletely resolved.
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Brain iron accumulation is well established in Alzheimers disease (AD), but whether the two share a genetic basis remains unclear.
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INTRODUCTIONAPOE*{varepsilon}4 is the strongest genetic risk factor for Alzheimers disease (AD), yet its effect varies across ancestral populations.
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In AβO-injected mice, AR, particularly at 200 mg/kg, attenuated memory deficits, reduced hippocampal neuronal degeneration, preserved synaptic protein immunoreactivity and increased markers of hippocampal cell proliferation and immature neurons.
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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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38/100
The study of Alzheimer's disease (AD)-associated mutations has implicated dysregulation of amyloid precursor protein (APP) proteolysis in the disease.
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= 0.032). In individuals with LOUE, elevated plasma p-tau217 was associated with both cognitive impairment and disrupted sleep microarchitecture, with the most pronounced cognitive deficits observed in individuals with medication refractory epilepsy.
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The purpose of this meta-analysis was to determine the common signature of dysregulated brain glucose metabolism in late-onset age-associated neurodegenerative diseases (A2NDs), including Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis.
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Polygenic and proteomic risk scores are both proposed for pre-symptomatic stratification, yet the extent to which they provide overlapping or complementary information has not been measured across neurodegenerative disease.
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Human leukocyte antigen (HLA) class II variation is implicated in Alzheimers disease (AD) and longevity, but its mechanisms within the major histocompatibility complex remain unclear.
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Copy-number variants (CNVs) are major contributors to human disease.
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Apolipoprotein E4 (APOE4) is a major risk factor for Alzheimer’s disease (AD).
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16/100
Alzheimers disease (AD) is defined by progressive neurodegeneration, yet a substantial fraction of its genetic risk maps to non-neuronal processes.
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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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Alzheimer disease (AD) pathology affects the transentorhinal/entorhinal region early but whether entorhinal cortex (EC) astrocytes are causal drivers or therapeutic targets remains unresolved.
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Genetic variation at the TMEM106B locus has been associated with Alzheimers disease (AD) and related neurodegenerative phenotypes, yet its haplotypic architecture remains incompletely resolved.
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16/100
Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood.
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Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus.
From across this tag
9 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 9. The same 9 appear here every time.
- Genetic association between intronic polymorphism in presenilin-1 gene and late-onset Alzheimer's disease. Alzheimer's Disease Collaborative Group
- N6-methyladenosine dynamics in neurodevelopment and aging, and its potential role in Alzheimer's disease
- APOE Genotype and Alzheimer's Disease: The Influence of Lifestyle and Environmental Factors
- APOE ε4 is associated with severity of Lewy body pathology independent of Alzheimer pathology
- Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer disease
- Exome sequencing reveals VCP mutations as a cause of familial ALS
- Possible involvement of advanced glycation end-products (AGEs) in the pathogenesis of Alzheimer's disease
- Plasma levels of Abeta42 and Abeta40 in Alzheimer patients during treatment with the acetylcholinesterase inhibitor tacrine
- Incidence of Alzheimer disease in a biracial urban community: relation to apolipoprotein E allele status