ArticleThe American journal of pathology2019
Apolipoprotein E/Amyloid-β Complex Accumulates in Alzheimer Disease Cortical Synapses via Apolipoprotein E Receptors and Is Enhanced by APOE4.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- APOE is a presynaptic protein that accumulates with age and modulates neurotransmitter release.bioRxiv : the preprint server for biology · 2026Article
- Identification of TMED10 as A Regulator for Neuronal Exocytosis of Amyloid Beta 42.Neuroscience bulletin · 2026Article
- Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) in Alzheimer's Disease: Recent Advances and Controversies.Molecular neurobiology · 2025Review
- Unraveling APOE4's Role in Alzheimer's Disease: Pathologies and Therapeutic Strategies.Current protein & peptide science · 2025Review
- Altered brain network dynamics and functional connectivity in subjective cognitive decline: an edge-centric network study.Frontiers in aging neuroscience · 2025Article
- Co-aggregation with Apolipoprotein E modulates the function of Amyloid-β in Alzheimer's disease.Nature communications · 2024Article
- Neuronal cell cycle reentry events in the aging brain are more prevalent in neurodegeneration and lead to cellular senescence.PLoS biology · 2024Article
- Cortical lipid metabolic pathway alteration of early Alzheimer's disease and candidate drugs screen.European journal of medical research · 2024Article
- Astrocyte-Neuron Interactions in Alzheimer's Disease.Advances in neurobiology · 2024Review
- Roles of ApoE4 on the Pathogenesis in Alzheimer's Disease and the Potential Therapeutic Approaches.Cellular and molecular neurobiology · 2023Review
- Apolipoprotein E intersects with amyloid-β within neurons.Life science alliance · 2023Article
- Reduced binding of apoE4 to complement factor H promotes amyloid-β oligomerization and neuroinflammation.EMBO reports · 2023Article
- Neuronal ApoE4 in Alzheimer's disease and potential therapeutic targets.Frontiers in aging neuroscience · 2023Review
- APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer's disease pathology and brain diseases.Molecular neurodegeneration · 2022Review
- Rapid and Gentle Immunopurification of Brain Synaptic Vesicles.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Tumor Apolipoprotein E is a key checkpoint blocking anti-tumor immunity in mouse melanoma.Frontiers in immunology · 2022Article
- Single-synapse analyses of Alzheimer's disease implicate pathologic tau, DJ1, CD47, and ApoE.Science advances · 2021Article
- Exosomal tau with seeding activity is released from Alzheimer's disease synapses, and seeding potential is associated with amyloid beta.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- A modified density gradient proteomic-based method to analyze endolysosomal proteins in cardiac tissue.iScience · 2021Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Apolipoprotein E (apoE) colocalizes with amyloid-β (Aβ) in Alzheimer disease (AD) plaques and in synapses, and evidence suggests that direct interactions between apoE and Aβ are important for apoE's effects in AD. The present work examines the hypothesis that apoE receptors mediate uptake of apoE/Aβ complex into synaptic terminals. Western blot analysis shows multiple SDS-stable assemblies in synaptosomes from human AD cortex; apoE/Aβ complex was markedly increased in AD compared with aged control samples. Complex formation between apoE and Aβ was confirmed by coimmunoprecipitation experiments. The apoE receptors low-density lipoprotein receptor (LDLR) and LDLR-related protein 1 (LRP1) were quantified in synaptosomes using flow cytometry, revealing up-regulation of LRP1 in early- and late-stage AD. Dual-labeling flow cytometry analysis of LRP1- and LDLR positives indicate most (approximately 65%) of LDLR and LRP1 is associated with postsynaptic density-95 (PSD-95)-positive synaptosomes, indicating that remaining LRP1 and LDLR receptors are exclusively presynaptic. Flow cytometry analysis of Nile red labeling revealed a reduction in cholesterol esters in AD synaptosomes. Dual-labeling experiments showed apoE and Aβ concentration into LDLR and LRP1-positive synaptosomes, along with free and esterified cholesterol. Synaptic Aβ was increased by apoE4 in control and AD samples. These results are consistent with uptake of apoE/Aβ complex and associated lipids into synaptic terminals, with subsequent Aβ clearance in control synapses and accumulation in AD synapses.
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Registered trials
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