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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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The objective of this study was to analyze factors influencing the risk and timing of Alzheimer's disease (AD) in central Norway.
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APOE epsilon 4 may influence rate of cognitive decline most significantly in the earliest stages of Alzheimer disease.
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Inflammation is associated with Abeta pathology in Alzheimer's disease (AD) and transgenic AD models.
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In this longitudinal study, impaired acute insulin response at midlife was associated with an increased risk of Alzheimer disease (AD) up to 35 years later suggesting a causal link between insulin metabolism and the pathogenesis of AD.
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58/100
Plasma A beta levels are affected by age and by systemic and CNS vascular risk factors.
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There is increasing evidence for blood-brain barrier (BBB) compromise in Alzheimer disease (AD).
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A majority of mutations within the beta-amyloid region of the amyloid precursor protein (APP) gene cause inherited forms of intracerebral hemorrhage.
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Alzheimer's disease is the commonest dementia.
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The major molecular risk factor for Alzheimer disease so far identified is the amyloidogenic peptide Abeta(42).
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50/100
Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult.
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The risk of dementia and Alzheimer's disease (AD) probably results from an interaction between genetic and environmental factors.
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These data are evidence of a gene x environment interaction for cognitive aging.
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51/100
APOE genotype is a major genetic risk factor for late-onset Alzheimer disease (AD).
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There is a great interest in the relationship between Mild Cognitive Impairment (MCI) and the progression to Alzheimer's disease (AD).
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67/100
Senile plaques accumulate over the course of decades in the brains of patients with Alzheimer's disease.
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Down-regulation of protein phosphatase 2A (PP2A) is thought to play a critical role in tau hyperphosphorylation in Alzheimer's disease (AD).
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The beta-amyloid peptide (Abeta) is the major constituent of the amyloid core of senile plaques found in the brain of patients with Alzheimer disease.
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Amyloid-beta (Abeta) peptide pathology in Alzheimer's disease (AD) comprises extracellular plaques and cerebral amyloid angiopathy (CAA).
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Numerous investigations point to the importance of oxidative imbalance in mediating AD pathogenesis.
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These data suggest that having both diabetes and APOE epsilon4 increases the risk of dementia, especially for AD and mixed AD.
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Alzheimer's disease (AD) is the most common cause of dementia in developed countries.
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MicroRNAs (miRNAs) are small regulatory RNAs that participate in posttranscriptional gene regulation in a sequence-specific manner.
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62/100
Unadjusted, SNP RS4420638 within APOC1 was strongly associated with AD due entirely to linkage disequilibrium with APOE.
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Alzheimer disease amyloid beta-peptide (Abeta) is generated via proteolytic processing of the beta-amyloid precursor protein by beta- and gamma-secretase.
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Of 214 participants, 48 showed no decline on any test, 126 showed decline on only 1 test in 1 or more domains, and 40 showed decline on 2 or more tests in 1 or more domains.
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Accumulating evidence suggests insulin and insulin signaling may be involved in the pathophysiology of Alzheimer disease (AD).
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Oxidative stress is thought to play a role in the pathogenesis of Alzheimer's disease (AD) and increased oxidative DNA damage has been observed in brain tissue from AD patients.
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Alzheimer disease is a common age-related neurodegenerative disease characterized pathologically by senile plaques, neurofibrillary tangles, synaptic disruption, and progressive neuronal deficits.
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Understanding the mechanisms of amyloid-beta protein (Abeta) production and clearance in the brain has been essential to elucidating the etiology of Alzheimer disease (AD).
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In a previous study, we found that human neural stem cells (HNSCs) exposed to high concentrations of secreted amyloid-precursor protein (sAPP) in vitro differentiated into mainly astrocytes, suggesting that pathological alterations in APP processing during neurodegenerative conditions such as Alzheimer's disease (AD) may prevent neuronal differentiation of HNSCs.
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The aspartyl protease beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) initiates processing of amyloid precursor protein (APP) into amyloid beta (Abeta) peptide, the major component of Alzheimer disease (AD) plaques.
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High dietary cholesterol and low dietary docosahexaenoic acid (DHA) intake are risk factors for Alzheimer's disease (AD).
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Mutation of the amyloid precursor protein (APP), presenilin-1, or presenilin-2 results in the development of early onset autosomal dominant forms of Alzheimer disease (AD).
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45/100
The amino acid sequence of amyloid precursor protein (APP) is highly conserved, and age-related A beta aggregates have been described in a variety of vertebrate animals, with the notable exception of mice and rats.
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Many proteins suspected of causing neurodegenerative diseases exist in diverse assembly states.
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The SPM analysis showed that patients with MCI had significantly higher [(11)C]PIB uptake vs control subjects in the frontal, parietal, and lateral temporal cortices as well as in the posterior cingulate showing the most prominent differences.
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These results strongly support the concept that synapse loss is a structural correlate involved very early in cognitive decline in mild Alzheimer disease (mAD) and supports mild cognitive impairment as a transitional stage between mAD and no cognitive impairment.
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Amyloid precursor protein (APP) metabolism is central to the pathogenesis of Alzheimer disease.
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The epsilon(4) allele of APOE confers a two- to fourfold increased risk for late-onset Alzheimer's disease (LOAD), but LOAD pathology does not all fit neatly around APOE.
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45/100
Mutations in presenilins are responsible for approximately 40% of all early-onset familial Alzheimer disease (FAD) cases in which a genetic cause has been identified.
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Selective increases in soluble Abeta(1-42) after TBI may predispose individuals with a brain injury to Alzheimer disease pathology.
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Alzheimer disease (AD) includes inflammatory processes in the senile plaques and surrounding glia, with increased expression of acute phase proteins such as C-reactive protein (CRP) and IL-6.
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This study confirms the association between genetic variants in SORL1 and AD.
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Microglia are the principal immune cells of the brain.
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A number of studies reported that oxidative and nitrosative damage may be important in the pathogenesis of Alzheimer's disease (AD).
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The plasma Abeta42/Abeta40 ratio may be a useful premorbid biomarker for identifying cognitively normal elderly white subjects who are at increased risk for developing MCI or AD.
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Advanced age and presence of intracerebral amyloid deposits are known to be major risk factors for development of neurodegeneration in Alzheimer's disease (AD), and both have been associated with microglial activation.
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46/100
Microglia are the main immune cells of the brain, and under some circumstances they can play an important role in removal of fibrillar Alzheimer amyloid beta peptide (fAbeta).
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Identification of preclinical markers is required for early diagnosis of Alzheimer's disease (AD) and cognitive dysfunction in advancing age.
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The somatodendritic accumulation of hyperphosphorylated tau proteins is an early event preceding the appearance of neurofibrillary tangles (NFT) in Alzheimer's disease (AD) and might be necessary for their formation.
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.
- Plaque-associated human microglia accumulate lipid droplets in a chimeric model of Alzheimer's disease
- Apolipoprotein E4 inhibits autophagy gene products through direct, specific binding to CLEAR motifs
- Apolipoprotein E Gene in α-Synucleinopathies: A Narrative Review
- β-Amyloid impairs axonal BDNF retrograde trafficking
- In silico structure-based multi-targeted molecular docking analysis of ginkgo biloba phytocompounds against Alzheimer’s disease associated proteins
- Amyloid precursor protein processing and retinal pathology in mouse models of Alzheimer's disease
- Apolipoprotein E: risk factor for Alzheimer disease
- Secretory processing of amyloid precursor protein is inhibited by increase in cellular cholesterol content
- alpha- and beta-secretase: profound changes in Alzheimer's disease
- Quantitative and Kinetic Proteomics Reveal ApoE Isoform-dependent Proteostasis Adaptations in Mouse Brain