ArticlePloS one2016
Differential Effects of apoE4 and Activation of ABCA1 on Brain and Plasma Lipoproteins.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- ABCA1: A Therapeutic Target for Improving Cholesterol Homeostasis in Peripheral Neuropathies.Biomolecules · 2026Review
- APOE-Targeted Therapeutics for Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Unraveling APOE4's Role in Alzheimer's Disease: Pathologies and Therapeutic Strategies.Current protein & peptide science · 2025Review
- Elevated lipopolysaccharide binding protein in Alzheimer's disease patients withFrontiers in neurology · 2024Article
- Effect of the ABCA1 agonist CS-6253 on amyloid-β and lipoprotein metabolism in cynomolgus monkeys.Alzheimer's research & therapy · 2022Article
- Remembering your A, B, C's: Alzheimer's disease and ABCA1.Acta pharmaceutica Sinica. B · 2022Review
- Neuronal ROS-induced glial lipid droplet formation is altered by loss of Alzheimer's disease-associated genes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Inflammatory Pathways Are Impaired in Alzheimer Disease and Differentially Associated With Apolipoprotein E Status.Journal of neuropathology and experimental neurology · 2021Article
- The Interplay of Apoes with Syndecans in Influencing Key Cellular Events of Amyloid Pathology.International journal of molecular sciences · 2021Article
- The Role of HDL and HDL Mimetic Peptides as Potential Therapeutics for Alzheimer's Disease.Biomolecules · 2020Review
- ApoE Lipidation as a Therapeutic Target in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- APOE in the normal brain.Neurobiology of disease · 2020Review
- Central and Peripheral Mechanisms in ApoE4-Driven Diabetic Pathology.International journal of molecular sciences · 2020Article
- Therapeutic approaches targeting Apolipoprotein E function in Alzheimer's disease.Molecular neurodegeneration · 2020Review
- The Important Interface Between Apolipoprotein E and Neuroinflammation in Alzheimer's Disease.Frontiers in immunology · 2020Review
- ApoE4: an emerging therapeutic target for Alzheimer's disease.BMC medicine · 2019Review
- Mitochondrial Cholesterol in Alzheimer's Disease and Niemann-Pick Type C Disease.Frontiers in neurology · 2019Review
- Cell-specific and region-specific transcriptomics in the multiple sclerosis model: Focus on astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The effects of apolipoprotein E genotype, α-synuclein deficiency, and sex on brain synaptic and Alzheimer's disease-related pathology.Alzheimer's & dementia (Amsterdam, Netherlands) · 2018Article
- Intracellular Cholesterol Trafficking and Impact in Neurodegeneration.Frontiers in molecular neuroscience · 2017Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein E4 (apoE4), the leading genetic risk factor for Alzheimer's disease (AD), is less lipidated compared to the most common and AD-benign allele, apoE3. We have recently shown that i.p. injections of the ATP-binding cassette A1 (ABCA1) agonist peptide CS-6253 to apoE mice reverse the hypolipidation of apoE4 and the associated brain pathology and behavioral deficits. While in the brain apoE is the main cholesterol transporter, in the periphery apoE and apoA-I both serve as the major cholesterol transporters. We presently investigated the extent to which apoE genotype and CS-6253 treatment to apoE3 and apoE4-targeted replacement mice affects the plasma levels and lipid particle distribution of apoE, and those of plasma and brain apoA-I and apoJ. This revealed that plasma levels of apoE4 were lower and eluted faster following FPLC than plasma apoE3. Treatment with CS-6253 increased the levels of plasma apoE4 and rendered the elution profile of apoE4 similar to that of apoE3. Similarly, the levels of plasma apoA-I were lower in the apoE4 mice compared to apoE3 mice, and this effect was partially reversed by CS-6253. Conversely, the levels of apoA-I in the brain which were higher in the apoE4 mice, were unaffected by CS-6253. The plasma levels of apoJ were higher in apoE4 mice than apoE3 mice and this effect was abolished by CS-6253. Similar but less pronounced effects were obtained in the brain. In conclusion, these results suggest that apoE4 affects the levels of apoA-I and apoJ and that the anti-apoE4 beneficial effects of CS-6253 may be related to both central and peripheral mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.