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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 apolipoprotein E (apoE) gene has been implicated in various conditions, most notably Alzheimer's disease and coronary artery disease.
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Apolipoprotein E4 (E4) and type 2 diabetes are major risk factors for cognitive decline and late onset Alzheimer's disease (AD).
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High-dose DHA supplementation in APOE4 carriers before the onset of AD dementia can be a promising approach to decrease the incidence of AD.
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Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci.
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APOE4 genotype is the strongest genetic risk factor for Alzheimer's disease.
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Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer's disease (AD).
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Alzheimer's disease (AD) is the most common cause of dementia, and its prevalence will increase significantly in the coming decades.
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Our data reveal an association of APOE ε3/3- TOMM40 '523 haplotypes with cognitive decline in community-based older persons such that the S/S poly-T genotype is related to faster cognitive decline, primarily in the domains of episodic and semantic memory.
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Human apolipoprotein E (ApoE) apolipoprotein is primarily expressed in three isoforms (ApoE2, ApoE3, and ApoE4) that differ only by two residues.
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As the population ages, neurodegenerative diseases such as Alzheimer's disease (AD) are becoming a significant burden on patients, their families, and health-care systems.
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In a cell free assay, ADAM10 activity was found to be significantly lower in apoE4 samples compared to apoE2. 7WCHO cells over expressing wild type AβPP exposed to apoE4 demonstrated reduced formation of sAβPPα compared to other apoE isoforms.
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These findings suggest amyloid pathologies significantly influence white matter and that these abnormalities may signify an early feature of the disease process.
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Among the 183 study participants, mean (SD) age was 85.5 (3) years, 76 were women (41.5%), and 177 were white (96.7%).
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In this study, altered AQP4 expression was associated with aging brains.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder, neuropathologically characterized by aggregates of β-amyloid peptides, which deposit as senile plaques, and of TAU protein, which forms neurofibrillary tangles.
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Soluble oligomers of amyloid β-protein (oAβ) isolated from the brains of Alzheimer's disease (AD) patients have been shown experimentally (in the absence of amyloid plaques) to impair hippocampal synaptic plasticity, decrease synapses, induce tau hyperphosphorylation and neuritic dystrophy, activate microglial inflammation, and impair memory in normal adult rodents.
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Neuropsychiatric symptoms are common manifestations of Alzheimer's disease (AD).
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Emerging evidence supports a role for innate immunity and microglia in Alzheimer's disease (AD) pathophysiology.
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Our results provide evidence supporting 25OHD as a causal risk factor for AD.
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Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression.
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Dementia is one of the major causes of disability in later life, and ischemic heart disease is a leading cause of morbidity and mortality.
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Alzheimer's disease (AD) is neuropathologically characterized by neuritic plaques and neurofibrillary tangles.
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Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E ε4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects.
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Alzheimer's disease (AD) is a neurodegenerative disease characterized by formation of amyloid-β (Aβ) plaques, activated microglia, and neuronal cell death leading to progressive dementia.
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In this study, serum DHA levels were associated with pathogenesis of cerebral amyloidosis and with preservation of entorhinal and hippocampal volumes.
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Alzheimer's disease (AD) is a gradually debilitating disease that leads to dementia.
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Alzheimer's disease (AD) is a devastating neurodegenerative disorder that causes progressive cognitive decline.
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Apolipoprotein E (apoE) is associated with lipoproteins in the cerebrospinal fluid (CSF).
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Efficient intercellular transfer of RNAs, proteins, and lipids as protected exosomal cargo has been demonstrated in the CNS, but distinct physiologic and pathologic roles have not been well defined for this pathway.
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We aimed to identify new candidate genes potentially involved in early-onset Alzheimer's disease (EOAD).
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Proteolysis of the amyloid precursor protein (APP) liberates various fragments including the proposed initiator of Alzheimer disease-associated dysfunctions, amyloid-β.
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The APOE gene is one of currently only two genes that have consistently been associated with longevity.
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Neurodegenerative diseases are distinguished by characteristic protein aggregates initiated by disease-specific 'seed' proteins; however, roles of other co-aggregated proteins remain largely unexplored.
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Apolipoprotein (apo) E was initially described as a lipid transport protein and major ligand for low density lipoprotein (LDL) receptors with a role in cholesterol metabolism and cardiovascular disease.
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Genetic risk factors for Alzheimer's disease imply that inflammation plays a causal role in development of the disease.
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The series of events underlying the pathogenesis of Alzheimer disease (AD) in unknown.
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In normal brain, neurons in the cortex and hippocampus produce insulin, which modulates glucose metabolism and cognitive functions.
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Men have a shorter life expectancy compared with women but the underlying factor(s) are not clear.
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Our findings suggest that the proposition that synaptic markers can predict cognitive decline in AD, should be extended to Lewy body diseases.
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This common ABCA7 deletion could represent an ethnic-specific pathogenic alteration in AD.
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ApoE on high-density lipoproteins is primarily responsible for lipid transport and cholesterol homeostasis in the central nervous system (CNS).
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The Alzheimer's disease risk gene apolipoprotein E epsilon 4 (APOE ε4) is associated with increased cerebral amyloid.
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In this study, we show that apoE lipoprotein particles from conditioned media of immortalized astrocytes isolated from human APOE-targeted replacement (TR) mice significantly suppress cellular Aβ42 and Aβ40 uptake through cell surface HSPG.
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55/100
This longitudinal study sought to determine whether the 18 kDa translocator protein (TSPO), a marker of neuroinflammation, increases over time in Alzheimer's disease.
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Carriers of the e4 allele may be more vulnerable to conditions that are independent risk factors for cognitive decline, such as cardiometabolic diseases.
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55/100
Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p Conclusions mI levels are elevated already at asymptomatic stages of AD.
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Higher HOMA-IR was associated with higher sAβPPβ and Aβ42 .
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Apolipoprotein E receptor 2 (ApoER2) is an apolipoprotein E receptor involved in long-term potentiation, learning, and memory.
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The lack of strong association between brain beta-amyloid deposition and cognitive impairment has been a challenge for the Alzheimer's disease (AD) field.
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Deposition of amyloid-β (Aβ) in the brain parenchyma and vessels is one of the hallmarks of Alzheimer disease (AD).
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.
- Amyloid precursor protein revisited: neuron-specific expression and highly stable nature of soluble derivatives
- Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease
- Advanced glycation end products contribute to amyloidosis in Alzheimer disease
- Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia
- Sex-specific effects of apolipoprotein E ε4 genotype on longitudinal hippocampal atrophy in amnestic mild cognitive impairment over a 2-year evaluation period
- Melatonin in Alzheimer's Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer's Neuropathology
- Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease
- Shifts in gut microbiota composition in an APP/PSS1 transgenic mouse model of Alzheimer's disease during lifespan
- Selective association of EEG microstates with clinical symptoms and mutation status in monogenic Alzheimer disease