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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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ABCA1 is an ATP-binding cassette protein that transports cellular cholesterol and phospholipids onto high density lipoproteins (HDL) in plasma.
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We examined the association of mtDNA variation with Alzheimer disease (AD) risk in Caucasians (989 cases and 328 controls) testing the effect of individual haplogroups and single nucleotide polymorphisms (SNPs).
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42/100
We compared lesions in elderly transgenic (tg) mice carrying the Swedish double mutation KM670/671NL with lesions in Alzheimer disease (AD) by histochemical and immunohistochemical techniques.
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We have previously shown that apolipoprotein E (Apoe) promotes the formation of amyloid in brain and that astrocyte-specific expression of APOE markedly affects the deposition of amyloid-beta peptides (Abeta) in a mouse model of Alzheimer disease.
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Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease.
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The epsilon4 allele of APOE is a risk factor for Alzheimer disease (AD).
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The APOE-4 allele increases risk and decreases age at onset of PD, an association that may not be dependent upon cognitive impairment.
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The epsilon4 allele does not predict cholinergic decline in AD.
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61/100
Memory declined in APOE e4 carriers before the symptomatic presentation of MCI in a cohort whose mean age was 60 years over a median period of 33 months.
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A change of the prion protein conformation results in a class of neurodegenerative diseases called the transmissible spongiform encephalopathies (like mad cow and Creutzfeld-Jakob diseases).
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Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding the microtubule-associated protein tau (MAPT).
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In Alzheimer disease (AD) patients, early memory dysfunction is associated with glucose hypometabolism and neuronal loss in the hippocampus.
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The extracellular accumulation of amyloid-beta (Abeta) in neuritic plaques is one of the characteristic hallmarks of Alzheimer's disease (AD), a progressive dementing neurodegenerative disorder of the elderly.
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The APOE epsilon4 allele acts as a potent risk factor for AD by accelerating onset.
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Amyloid plaques appear early during Alzheimer's disease (AD), and their development is intimately linked to activated astrocytes and microglia.
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Synaptic damage and loss are factors that affect the degree of dementia experienced in Alzheimer disease (AD) patients.
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Alzheimer disease (AD) involves glial inflammation associated with amyloid plaques.
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43/100
Beta-amyloid peptides that are cleaved from the amyloid precursor protein (APP) play a critical role in Alzheimer's disease (AD) pathophysiology.
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Nosologically, Alzheimer disease is not a single disorder in spite of a common clinical phenotype.
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Increasing evidence indicates that there are reductions in estrogen and androgen levels in aged men and women.
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57/100
These data support distinct processes in the initiation and progression of AD pathology within the temporal cortex: Deposition of Abeta reaches a "ceiling" early in the disease process, whereas NFT formation, synaptic loss, and gliosis continue throughout the course of the illness.
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Longitudinal clinicopathologic cohort study.
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Apolipoprotein E (apoE) is found in amyloid plaques and neurofibrillary tangles (NFTs) in Alzheimer's disease (AD) brains, but its role in their pathogenesis is unclear.
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This study questions the effect of statins on the processing of amyloid precursor protein in humans.
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Although an immense knowledge has accumulated concerning regulation of cholesterol homeostasis in the body, this does not include the brain, where details are just emerging.
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The binding of amyloid beta peptides (Abeta) to plasma membranes appears to be a promising point of intervention in the events leading to the development of Alzheimer's disease (AD).
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Amyloid precursor protein (APP), ADAM 10, and beta-site-APP cleaving enzyme (BACE) alterations were evaluated in platelets of 31 patients with Alzheimer disease (AD) and 15 age-matched controls.
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Chronically activated glia associated with amyloid plaques might contribute to neuronal dysfunction in Alzheimer's disease (AD) through generation of neuroinflammatory molecules.
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Alzheimer disease is not a single disorder.
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Converging evidence suggests that the accumulation of cerebral amyloid beta-protein (Abeta) in Alzheimer's disease (AD) reflects an imbalance between the production and degradation of this self-aggregating peptide.
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Epidemiological studies of Alzheimer patients from a wide variety of ethnic and socioeconomic backgrounds have identified education and occupation as environmental factors that can affect the risk of developing disease.
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Abnormal cleavage of amyloid precursor protein (APP) in the central nervous system has been linked to the development of Alzheimer's disease.
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Immunostaining of adenosine receptors in the hippocampus and cerebral cortex from necropsies of Alzheimer disease (AD) patients shows that there is a change in the pattern of expression and a redistribution of receptors in these brain areas when compared with samples from controls.
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We conducted a quantitative investigation of brain arterial atherosclerotic damage and its relationship to sporadic Alzheimer's disease (AD).
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Cerebral amyloid angiopathy (CAA) is a feature of ageing and Alzheimer's disease (AD); it is also associated with intracerebral hemorrhage and stroke.
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One of the major histopathological hallmarks of Alzheimer's disease (AD) is redundant senile plaques mainly composed of beta-amyloid (Abeta) aggregates.
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Glial fibrillary acidic protein (GFAP) is considered to be a highly specific marker for glia.
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Apoptotic pathways and DNA synthesis are activated in neurons in the brains of individuals with Alzheimer disease (AD).
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51/100
Serum hypercholesterolemia may be an early risk factor for the development of AD amyloid pathology.
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Researchers derived a triple-transgenic model to study the interaction between Abeta and tau and their effect on synaptic function.
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Alzheimer's dementia (AD) is the most common degenerative disorder of the central nervous system.
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48/100
Inheritance of the APOE epsilon4 allele is associated with increased risk of late posttraumatic seizures.
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Vaccination against human beta-amyloid peptide (A beta) has been shown to remove the amyloid burden produced in transgenic mice overexpressing the mutated human amyloid precursor protein (APP) gene.
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beta-Amyloid(1-42) (A beta 42), a major component of amyloid plaques, accumulates within pyramidal neurons in the brains of individuals with Alzheimer's disease (AD) and Down syndrome.
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In this large, population-based cohort, baseline and long-term average serum total cholesterol levels were not associated with the risk for incident AD.
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A hallmark of all forms of Alzheimer's disease (AD) is an abnormal accumulation of the beta-amyloid protein (Abeta) in specific brain regions.
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52/100
Low n-3 polyunsaturated fatty acid (PUFA) status may be associated with neuro-degenerative disorders, in particular Alzheimer's disease, which has been associated with poor dietary fish or n-3 PUFA intake, and low docosahexaenoic acid (DHA) status.
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Presenilin 1 (PS1) is a key factor for beta-amyloid (Ab) formation in Alzheimer disease (AD).
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Amyloid-beta peptide (Abeta) has a key role in the pathogenesis of Alzheimer disease (AD).
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Apolipoprotein E epsilon4 led to increased risk of AD among white subjects but not black subjects.
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.
- Interaction of Glucagon-Like Peptide 1 and Its Analogues with Amyloid-β Peptide Affects Its Fibrillation and Cytotoxicity
- Dephosphorylation of Alzheimer paired helical filaments by protein phosphatase-2A and -2B
- A genome-wide association meta-analysis of plasma Aβ peptides concentrations in the elderly
- Sex-Specific Cross Tissue Meta-Analysis Identifies Immune Dysregulation in Women With Alzheimer's Disease
- Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease
- Small-Molecule Inhibitors of Amyloid Beta: Insights from Molecular Dynamics—Part B: Natural Compounds
- Lack of an association of estrogen receptor alpha gene polymorphisms and transcriptional activity with Alzheimer disease
- Anti-amyloid antibody equilibrium binding to Aβ aggregates from human Alzheimer disease brain
- APP antisense oligonucleotides reduce amyloid-β aggregation and rescue endolysosomal dysfunction in Alzheimer's disease
- The Alzheimer amyloid precursor protein. Identification of a stable intermediate in the biosynthetic/degradative pathway