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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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EOAD, although sharing genes with LOAD, harbors unique genes and pathways that could be used to create better prediction models or target identification.
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Cross-sectional studies suggest a limited relationship between accelerated epigenetic aging derived from epigenetic clocks, and Alzheimer's disease (AD) pathophysiology or risk.
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16/100
Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E).
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Our results show that genotype, AOF, and sex contributed to AD-like pathology.
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BACKGROUNDTraffic-related air pollution (TRAP) is a risk factor for Alzheimer disease (AD), where unresolved brain inflammation has been linked to deficits in the levels of free lipid mediators that enable the resolution of inflammation.
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Alzheimer's disease (AD) diagnosis relies on cerebrospinal fluid (CSF) biomarkers or amyloid PET.
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value = 0.04). ε4 on cognition is mediated by structural brain imaging markers, driven mainly by cerebral microbleeds.
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Although apolipoprotein E (ApoE) ε4 is a well-established risk factor for Alzheimer disease, its role in the development of post-stroke cognitive impairment (PSCI) remains uncertain.
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Growing evidence highlights sex-related differences in the pathogenesis of Alzheimer's disease (AD).
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Apolipoprotein E (ApoE) variants are central to Alzheimer's disease (AD), Lewy body dementia (LBD) and Niemann-Pick disease type C (NPC).
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Neurodegenerative disorders such as Alzheimer's disease (AD), the most common form of dementia, represent a growing global health crisis, yet current treatment strategies remain primarily palliative.
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Alzheimer's disease (AD) is the most common cause of dementia.
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Biallelic loss-of-function variants in TYROBP and TREM2 cause autosomal recessive presenile dementia with bone cysts known as Nasu-Hakola disease (NHD, alternatively polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, PLOSL).
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Clinical data, animal and cell studies show that some antidiabetic drugs, including glucagon-like peptide 1 receptor agonists (GLP-1RAs), exert therapeutic effects in Alzheimer's disease (AD) via modulation of amyloid-β peptide (Aβ) metabolism.
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The ApoE-ε4 gene is a well-established genetic risk factor for neurodegenerative diseases, such as Alzheimer's disease and multiple sclerosis, which are characterized by axonal demyelination in the central nervous system.
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APOE shows a heterogeneous effect on ADRD risk in our Hispanics/Latinos sample, the largest to date.
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• Low ALPS index was significantly associated with high risk of MCI, and the risk of MCI decreased linearly with a higher ALPS index • High ALPS index was dose-dependently associated with a decreased progression from MCI to AD • High ALPS index may delay the MCI onset approximately 3.8 years among CN participants and delay MCI progression to AD by approximately 3.5 years in MCI group • Aβ in choroid plexus, tau in part of the cortex and executive function were partially mediate ALPS-AD association We aimed to explore the association between ALPS index and both risks of MCI from cognitively normal (CN) and incident AD progressed from MCI, as well as potential mediating factors.
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This report highlights a case of relapsing remitting rapidly progressive dementia due to cerebral amyloid angiopathy-related inflammation (CAA-ri), focusing on the diagnostic challenges and the dramatic response to corticosteroid treatment.
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Alzheimer's disease (AD) is a predominant form of dementia in elderly.
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Our findings revealed significantly elevated CSF GAP-43 levels in individuals with AD compared to CN and MCI groups.
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The first search utilized the following MeSH terms and keywords: ‘Plasma Exchange’, ‘Plasmapheresis’, ‘Therapeutic plasma exchange’, ‘Apheresis’, ‘Aβ’, ‘p-tau’, ‘Total-tau’, ‘Alzheimer's disease’, ‘Cognitive dysfunction’, ‘neurodegenerative diseases’, ‘centrifugation’, ‘membranous’, and ‘filtration’ in the Title/Abstract, yielding 146 results.
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Alzheimer's disease (AD) involves a dynamic interaction between neuroinflammation and metabolic dysregulation, where microglia play a central role.
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BackgroundTo date, cholinomimetics remain central in the pharmacotherapy of Alzheimer's disease (AD) dementia.
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Alzheimer's disease currently has no cure and is usually detected too late for interventions to be effective.
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The apolipoprotein E (APOE) gene is the strongest genetic risk modifier for Alzheimer's disease (AD), with the APOE4 allele increasing risk and APOE2 decreasing it compared with the common APOE3 allele.
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The genetic component of early-onset Alzheimer disease (EOAD), accounting for ~10% of all Alzheimer's disease (AD) cases, is largely unexplained.
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Alzheimer's disease (AD) is an age-associated neurodegenerative disorder with a complex etiology.
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35/100
Alzheimer's disease (AD) is a multifactorial disorder associated with neuroinflammation, elevated oxidative stress, lipid alterations as well as amyloid-deposits and the formation of neurofibrillary tangles.
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Alzheimer's disease (AD), a leading cause of dementia worldwide, is a multifactorial neurodegenerative disorder characterized by amyloid-beta plaques, tauopathy, neuronal loss, neuro-inflammation, brain atrophy, and cognitive deficits.
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65/100
Alzheimer's disease (AD) therapies utilizing amyloid-β (Aβ) immunization have shown potential in clinical trials.
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Age, sex, and apolipoprotein E (APOE) are the strongest risk factors for late-onset Alzheimer disease (AD).
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The CU- group had lower baseline GAP-43 than all Aβ+ groups, but not the other Aβ- groups.
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Trisomy of chromosome 21, the cause of Down syndrome (DS), is the most commonly occurring genetic cause of Alzheimer’s disease (AD).
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Alzheimer's disease (AD) is a common and increasing societal problem due to the extending human lifespan.
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The amyloid hypothesis is the predominant model of Alzheimer's disease (AD) pathogenesis, suggesting that amyloid beta (Aβ) peptide is the primary driver of neurotoxicity and a cascade of pathological events in the central nervous system.
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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss and cognitive decline, with women being disproportionately affected in both prevalence and severity.
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Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis.
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Amyloidoses, which are characterized by abnormal accumulation of amyloid proteins leading to organ dysfunction, represent a major therapeutic challenge.
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H]UCB-J was found to be reduced in frontal cortex from patients with AD.
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We identified that the APOE4 genotype affected ΔHV in females.
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Previous studies have suggested that systemic viral infections may increase risks of dementia.
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Genetic diversity in the apolipoprotein E (ApoE) gene has been identified as the major susceptibility genetic risk factor for sporadic Alzheimer’s disease (SAD).
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Copy number variation (CNV) of the amyloid-β precursor protein gene (APP) is a known cause of autosomal dominant Alzheimer disease (ADAD), but de novo genetic variants causing ADAD are rare.
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APP/PS1 mice at 6 months were randomly allocated to two dietary groups: one receiving ad libitum (AL) feeding and the other undergoing IF for 1 month.
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Neural autoantibodies are being increasingly detected in conjunction with neurodegenerative dementias such as Alzheimer's disease dementia (AD), yet their significance is not well clarified.
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Metabolomics provide a promising tool for understanding dementia pathogenesis and identifying novel biomarkers.
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Although the relationship between macroautophagy/autophagy and Alzheimer disease (AD) is widely studied, the underlying mechanisms are poorly understood, especially the regulatory role of the initiation signaling of autophagy on AD.
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-heterozygous human brain tissue was reactivated in response to neuroinflammation caused by exposure to other pathogens.
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Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear.
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APOE4-KI mice showed impaired retinal structure, vasculature, function, vision, increased gliosis and neuroinflammation, and downregulation of synaptogenesis.
From across this tag
9 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 9. The same 9 appear here every time.
- Single-nucleus RNA-sequencing of autosomal dominant Alzheimer disease and risk variant carriers
- Brain cholesterol: long secret life behind a barrier
- Amyloid deposition and influx transporter expression at the blood-brain barrier increase in normal aging
- Alpha 1-antichymotrypsin binding to Alzheimer A beta peptides is sequence specific and induces fibril disaggregation in vitro
- Patients with Alzheimer disease have lower levels of serum anti-amyloid peptide antibodies than healthy elderly individuals
- Mechanisms behind the neuroprotective actions of cholinesterase inhibitors in Alzheimer disease
- Alzheimer‐related neuropathology is improved by treatment with longevity‐enhancing treatments in aged male EFAD mice
- Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E
- Cerebrovascular effects of apolipoprotein E: implications for Alzheimer disease