ArticleNature chemistry2018
Inhibiting amyloid-β cytotoxicity through its interaction with the cell surface receptor LilrB2 by structure-based design.
Article in Nature chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
What it found
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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.
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
38 citing papers in PubMed.
- Ethnic-specific effects of the LILRB2-LILRB5 locus and newly identified risk loci for Alzheimer's disease in the East Asian population.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Co-expression-wide association studies link genetically regulated interactions with complex traits.Nature communications · 2025Article
- C4d, a high-affinity LilrB2 ligand, is elevated in Alzheimer's disease and mediates synapse pruning.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The role of inhibitory immune checkpoint receptors in the pathogenesis of Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Article
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
- Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies.Signal transduction and targeted therapy · 2024Review
- Immune receptors and aging brain.Bioscience reports · 2024Review
- Misfolded protein oligomers: mechanisms of formation, cytotoxic effects, and pharmacological approaches against protein misfolding diseases.Molecular neurodegeneration · 2024Review
- Autophagy-lysosomal pathway impairment and cathepsin dysregulation in Alzheimer's disease.Frontiers in molecular biosciences · 2024Review
- Fibrinogen induces inflammatory responses via the immune activating receptor LILRA2.Frontiers in immunology · 2024Article
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- Amyloid-β in Alzheimer's disease: Structure, toxicity, distribution, treatment, and prospects.Ibrain · 2024Review
- Simulations of Amyloid-Forming Peptides in the Crystal State.The protein journal · 2023Article
- An Insight into Cellular and Molecular Mechanisms Underlying the Pathogenesis of Neurodegeneration in Alzheimer's Disease.Biomedicines · 2023Review
- Novel approaches to increase synaptic resilience as potential treatments for Alzheimer's disease.Seminars in cell & developmental biology · 2023Review
- Human leukocyte immunoglobulin-like receptors in health and disease.Frontiers in immunology · 2023Review
- LOTUS suppresses amyloid β-induced dendritic spine elimination through the blockade of amyloid β binding to PirB.Molecular medicine (Cambridge, Mass.) · 2022Article
- Identifying Rare Genetic Variants of Immune Mediators as Risk Factors for Autism Spectrum Disorder.Genes · 2022Article
- LILRB2-mediated TREM2 signaling inhibition suppresses microglia functions.Molecular neurodegeneration · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
Abstract
Inhibiting the interaction between amyloid-β (Aβ) and a neuronal cell surface receptor, LilrB2, has been suggested as a potential route for treating Alzheimer's disease. Supporting this approach, Alzheimer's-like symptoms are reduced in mouse models following genetic depletion of the LilrB2 homologue. In its pathogenic, oligomeric state, Aβ binds to LilrB2, triggering a pathway to synaptic loss. Here we identify the LilrB2 binding moieties 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.