ArticleProteins2011
A differential association of Apolipoprotein E isoforms with the amyloid-β oligomer in solution.
Article in Proteins, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed.
- Recent Advances in the Treatment and Management of Alzheimer's Disease: A Precision Medicine Perspective.Current topics in medicinal chemistry · 2024Review
- Construction of an Exudative Age-Related Macular Degeneration Diagnostic and Therapeutic Molecular Network Using Multi-Layer Network Analysis, a Fuzzy Logic Model, and Deep Learning Techniques: Are Retinal and Brain Neurodegenerative Disorders Related?Pharmaceuticals (Basel, Switzerland) · 2023Article
- Apolipoprotein E4 has extensive conformational heterogeneity in lipid-free and lipid-bound forms.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Low-Density Lipoprotein Receptor-Related Protein 8 at the Crossroad between Cancer and Neurodegeneration.International journal of molecular sciences · 2022Review
- Antibacterial and Anti-Inflammatory Effects of Apolipoprotein E.Biomedicines · 2022Article
- Are apolipoprotein E fragments a promising new therapeutic target for Alzheimer's disease?Therapeutic advances in chronic disease · 2022Review
- Interactions between Apolipoprotein E Metabolism and Retinal Inflammation in Age-Related Macular Degeneration.Life (Basel, Switzerland) · 2021Review
- Apolipoprotein E Polymorphism and Oxidative Stress in Peripheral Blood-Derived Macrophage-Mediated Amyloid-Beta Phagocytosis in Alzheimer's Disease Patients.Cellular and molecular neurobiology · 2019Article
- Cerebrospinal Fluid Proteins as Regulators of Beta-amyloid Aggregation and Toxicity.Israel journal of chemistry · 2017Article
- Aggregation of thrombin-derived C-terminal fragments as a previously undisclosed host defense mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Interaction of the amyloid β peptide with sodium dodecyl sulfate as a membrane-mimicking detergent.Journal of biological physics · 2016Article
- Clusterin Binds to Aβ1-42 Oligomers with High Affinity and Interferes with Peptide Aggregation by Inhibiting Primary and Secondary Nucleation.The Journal of biological chemistry · 2016Article
- Protective spin-labeled fluorenes maintain amyloid beta peptide in small oligomers and limit transitions in secondary structure.Biochimica et biophysica acta · 2015Article
- Role of apolipoprotein E in neurodegenerative diseases.Neuropsychiatric disease and treatment · 2015Review
- Tomoregulin (TMEFF2) Binds Alzheimer's Disease Amyloid-β (Aβ) Oligomer and AβPP and Protects Neurons from Aβ-Induced Toxicity.Journal of Alzheimer's disease : JAD · 2015Article
- Apolipoprotein E, amyloid-beta, and neuroinflammation in Alzheimer's disease.Neuroscience bulletin · 2014Review
- Review
- Soluble apoE/Aβ complex: mechanism and therapeutic target for APOE4-induced AD risk.Molecular neurodegeneration · 2014Review
- Mapping the interactions between the Alzheimer's Aβ-peptide and human serum albumin beyond domain resolution.Biophysical journal · 2013Article
- Antimitochondrial antibody recognition and structural integrity of the inner lipoyl domain of the E2 subunit of pyruvate dehydrogenase complex.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The molecular pathogenesis of disorders arising from protein misfolding and aggregation is difficult to elucidate, involving a complex ensemble of intermediates, whose toxicity depends upon their state of progression along distinct processing pathways. To address the complex misfolding and aggregation that initiates the toxic cascade resulting in Alzheimer's disease (AD), we have developed a 2,2,6,6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid spin-labeled amyloid-β (Aβ) peptide to observe its isoform-dependent interaction with the apoE protein. Although most individuals carry the E3 isoform of apoE, ∼15% of humans carry the E4 isoform, which is recognized as the most significant genetic determinant for Alzheimer's. ApoE is consistently associated with the amyloid plaque marker for AD. A vital question centers on the influence of the two predominant isoforms, E3 and E4, on Aβ peptide processing and hence Aβ toxicity. We used electron paramagnetic resonance (EPR) spectroscopy of incorporated spin labels to investigate the interaction of apoE with the toxic oligomeric species of Aβ in solution. EPR spectra of the spin-labeled side chain report on side chain and backbone dynamics as well as the spatial proximity of spins in an assembly. Our results indicate oligomer binding involves the C-terminal domain of apoE, with apoE3 reporting a much greater response through this conformational marker. Coupled with SPR binding measurements, apoE3 displays a higher affinity and capacity for the toxic Aβ oligomer. These findings support the hypothesis that apoE polymorphism and Alzheimer's risk can largely be attributed to the reduced ability of apoE4 to function as a clearance vehicle for the toxic form of Aβ.
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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.