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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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Apolipoprotein E (APOE) dependent lifetime risks (LTRs) for Alzheimer Disease (AD) are currently not accurately known and odds ratios alone are insufficient to assess these risks.
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It has long been assumed that β-amyloid (Aβ) had to assemble into fibrillar amyloid plaques to exert its neurotoxic effects in Alzheimer disease.
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One third of patients with pathologic confirmed EOAD presented with atypical symptoms.
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67/100
The APOE-ε4 allele is associated with a moderately increased risk for progression from MCI to AD-type dementia.
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Disruption of functional connectivity between brain regions may represent an early functional consequence of β-amyloid pathology prior to clinical Alzheimer's disease.
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The goal of this study was to investigate the role of endogenous amyloid-β peptide (Aβ) in healthy brain.
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The authors sought to identify new susceptibility loci for Alzheimer's disease through a staged association study and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium in a companion paper.
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The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3).
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Neurotrophins, activating the PI3K/Akt signaling pathway, control neuronal survival and plasticity.
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49/100
No frontal cognitive effects were as robust as memory decline.
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Lipid-mediated signalling regulates a plethora of physiological processes, including crucial aspects of brain function.
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The incidence of Alzheimer disease (AD) and diabetes mellitus (DM) is increasing at an alarming rate and has become a major public health concern worldwide.
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Two multicentre genome-wide association (GWA) studies provided substantial evidence, implicating the complement receptor 1 gene (CR1) in Alzheimer disease (AD) genetic etiology.
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Analysis of cross-sectional data from the AIBL study indicates that plasma apoE levels are altered in AD and correlate with AD pathology level.
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49/100
The sirtuin pathway, which is most notable for its association with the anti-ageing effects of calorie restriction, has received particular attention, and pharmacological or transgenic upregulation of the sirtuin pathway has shown promising results in laboratory models of ageing.
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Recent GWAS studies focused on uncovering novel genetic loci related to AD have revealed associations with variants near CLU, CR1, PICALM and BIN1.
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Late-onset Alzheimer's disease (LOAD) is the most common form of dementia in the elderly.
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Alzheimer disease is characterized by accumulation of the β-amyloid peptide (Aβ) generated by β- and γ-secretase processing of the amyloid precursor protein (APP).
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Alzheimer's disease (AD) is a neurodegenerative disease with major clinical hallmarks of memory loss, dementia, and cognitive impairment.
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Representing the most common cause of dementia, Alzheimer's disease (AD) has dramatically impacted the neurological and economic health of our society.
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The association of rs1990622 with AAO explains, in part, the wide range in the AAO of disease among GRN mutation carriers.
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Since the discovery of the association of apolipoprotein E (apoE) 4 with Alzheimer's disease 17 years ago, numerous in vitro experiments with the apoE isoforms (apoE2, apoE3, and apoE4) have been performed to try to understand the basis for this association.
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Comprehensive and unbiased meta-analysis of all published and unpublished data from case-control studies for the SORL1 single-nucleotide polymorphisms (SNPs) that had been repeatedly assessed across studies.
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Plasma sphingolipids have been shown to predict cognitive impairment and hippocampal volume loss, but there is little research in patients with Alzheimer's disease (AD).
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51/100
Niemann-Pick disease type C (NPC) is an inherited disorder characterized by intracellular accumulation of lipids such as cholesterol and glycosphingolipids in endosomes and lysosomes.
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The significance of the cerebrospinal fluid (CSF) Apolipoprotein E (APOE) level and whether it might have differential effects on brain function due to the presence of APOE ε 4 allele(s) in HIV-infected patients are unknown.
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Using exome sequencing, we identified a p.R191Q amino acid change in the valosin-containing protein (VCP) gene in an Italian family with autosomal dominantly inherited amyotrophic lateral sclerosis (ALS).
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Apolipoprotein (apo) E4 is the major genetic risk factor for late-onset Alzheimer disease (AD).
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Amyloid-β oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2.
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Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia.
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Our genome-wide search of Caribbean Hispanic individuals identified several novel genetic variants associated with LOAD and replicated these associations in a white cohort.
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Our findings suggest that insulin metabolism influences the clinical manifestation of AD only within 3 years.
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Recent studies indicate that the deposition of β-amyloid peptide (Aβ) is related to the pathogenesis of Alzheimer disease (AD); however, the underlying mechanism is still not clear.
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Deposition of amyloid β (Aβ) in the brain is closely associated with Alzheimer disease (AD).
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36/100
Soluble oligomeric aggregates of the amyloid-beta (A beta) peptide are believed to be the most neurotoxic A beta species affecting the brain in Alzheimer disease (AD), a terminal neurodegenerative disorder involving severe cognitive decline underscored by initial synaptic dysfunction and later extensive neuronal death in the CNS.
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Reduced clearance of amyloid β peptides (Aβ) across the blood-brain barrier contributes to amyloid accumulation in Alzheimer disease.
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This study suggests that both tHcy and holoTC may be involved in the development of AD.
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The frequencies of individual ApoE genotypes did not differ between patients with ALS and ALS-free Caucasian populations.
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Genome-wide association studies (GWAS) of late-onset Alzheimer disease (LOAD) have consistently observed strong evidence of association with polymorphisms in APOE.
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The BACE1 gene encodes the beta-site APP-cleaving enzyme 1 and has been associated with Alzheimer's disease (AD).
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BPs of [(11)C](R)PK11195 and [(11)C]PIB were significantly higher in the parietotemporal regions of AD patients than in ten healthy controls.
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To date there is no effective therapy for Alzheimer disease (AD).
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A hallmark of Alzheimer disease (AD) is the deposition of amyloid β (Aβ) in brain parenchyma and cerebral blood vessels, accompanied by cognitive decline.
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The results of this study suggest that hyperinsulinemia and hyperglycemia caused by insulin resistance accelerate NP formation in combination with the effects of APOE epsilon4.
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We confirm in a completely independent data set that CR1, CLU, and PICALM are AD susceptibility loci in European ancestry populations.
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46/100
Recent evidence suggests that high molecular weight soluble oligomeric Abeta (oAbeta) assemblies (also known as Abeta-derived diffusible ligands, or ADDLs) may represent a primary neurotoxic basis for cognitive failure in Alzheimer disease (AD).
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The purpose of this review is to provide insights into recent advances in mechanisms linking apolipoprotein (apo) E isoforms to cardiovascular and neurological diseases.
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These data support the hypothesis that neuronal endosomal dysfunction is associated with preclinical AD.
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We examined longitudinal associations between the apolipoprotein E ε4 allele (ApoE4(+) status) and several cognitive outcomes and tested effect modification by sex.
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.
- Red blood cell ω-3 status and longitudinal cognition in individuals at risk of Alzheimer disease
- The interplay of PICALM with APOE ε4 on Alzheimer’s disease: clues from two longitudinal cohorts and proteomic studies
- Combating Genetic Heterogeneity for Polygenic Prediction of Susceptibility to Brain β-Amyloid Deposition
- APOE4 exacerbates α-synuclein pathology and related toxicity independent of amyloid
- Longitudinal changes in cognition and behavior in asymptomatic carriers of the APOE e4 allele
- Apolipoprotein E as vascular risk factor in neurodegenerative dementia
- Morphologic association between microglia and senile plaque amyloid in Alzheimer's disease
- Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease
- Increased monoamine oxidase B activity in plaque-associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography
- Altered expression of genes for amyloid and cytoskeletal proteins in Alzheimer cortex