25 results for “apoe4”. Showing 25 of 39,449.
Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer disease.
apoE4 (NSE-apoE4) transgenic mice. All subunits of mitochondrial respiratory
A novel conditional knock-in mouse model for APOE4-to-APOE3 switching.
APOE4-FLEx 4-to-3 construct to generate APOE4-FLEx
APOE4 disrupts intracellular lipid homeostasis in human iPSC-derived glia.
APOE4 disrupts intracellular lipid homeostasis in human iPSC-derived glia
APOE4 impairs myelination via cholesterol dysregulation in oligodendrocytes.
APOE4 carriers compared with non-carriers. This revealed that APOE4
Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function.
apoE4 or apoE3. Under basal conditions, apoE4 impaired respiration and increased
APOE4, Blood Neurodegenerative Biomarkers, and Cognitive Decline in Community-Dwelling Older Adults.
APOE4 carriers than noncarriers. Specifically, compared with noncarriers, APOE4 carriers
ApoE4 Alters ABCA1 Membrane Trafficking in Astrocytes.
ApoE4 protein is prone to aggregate and lipidating ApoE4 protects
Group 1 mGluR stimulation rescues APOE4-mediated translation defects in neurons.
APOE4) is the most recognized risk factor for Alzheimer's disease
Quantitative Assessment of Conformational Heterogeneity in Apolipoprotein E4 Using Hydrogen-Deuterium Exchange Mass Spectrometry.
apoE4) is the strongest genetic risk factor for Alzheimer's disease
From Genetics to Neuroinflammation: The Impact of ApoE4 on Microglial Function in Alzheimer's Disease.
ApoE4) allele is the most prominent genetic risk factor for late
Alteration in oral and non-oral tissues in ligature-induced periodontitis mice with the Alzheimer's disease risk factor APOE4.
APOE4-knockin, APOE4-knockin with periodontitis, infliximab-treated periodontitis, and infliximab
APOE4 leads to blood-brain barrier dysfunction predicting cognitive decline.
APOE4 leads to blood-brain barrier dysfunction predicting cognitive decline
Reversal of ApoE4-Driven Brain Pathology by Vascular Endothelial Growth Factor Treatment.
ApoE4), the most prevalent genetic risk factor for Alzheimer's disease
ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism.
ApoE4 diminishing the transport efficiency. Further, ApoE4 lowers FA oxidation
Astrocytic APOE4 removal confers cerebrovascular protection despite increased cerebral amyloid angiopathy.
APOE4 was removed from astrocytes of 5XFAD APOE4 knock-in mice
In Silico Analysis of the Antagonist Effect of Enoxaparin on the ApoE4-Amyloid-Beta (A
ApoE4-interacting sites and thus can neutralize or disrupt ApoE4
Astrocyte-secreted glypican-4 drives APOE4-dependent tau hyperphosphorylation.
APOE4), the highest genetic risk factor for late-onset AD, has been
APOE4 Causes Widespread Molecular and Cellular Alterations Associated with Alzheimer's Disease Phenotypes in Human iPSC-Derived Brain Cell Types
APOE4) variant is the single greatest genetic risk factor for sporadic
Cell type-specific roles of APOE4 in Alzheimer disease.
APOE4 cascade model of AD. In this model, neuronal APOE4
APOE4 impairs the microglial response in Alzheimer's disease by inducing TGFβ-mediated checkpoints.
APOE4 deletion. In the brains of AD donors carrying the APOE4
Lysosomal proteomics reveals mechanisms of neuronal APOE4-associated lysosomal dysfunction.
APOE4 localizes to lysosomes, the influence of APOE4 on lysosomal
APOE4 reduces hippocampal expression of phosphoglycerate kinase 1 and sodium potassium pump to enhance seizure susceptibility in mice.
APOE4, the major genetic risk factor of AD. However, the mechanism
Apolipoprotein E: from cardiovascular disease to neurodegenerative disorders.
apoE4), which differ by only a single amino acid interchange
Modest neurodevelopment impacts of APOE4 in a human brain organoid model of low-grade SARS-CoV-2 infection.
APOE4-dependent changes. In infected COs, APOE4 elevated immature astrocyte
The APOE-R136S mutation protects against APOE4-driven Tau pathology, neurodegeneration and neuroinflammation.
APOE4) is the strongest genetic risk factor for late-onset