ArticleThe EMBO journal2022
Heterotypic Amyloid β interactions facilitate amyloid assembly and modify amyloid structure.
Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- TAF15 amyloids propagate via defined motifs in a prion-like fashion.Nature communications · 2026Article
- Atomic structures of medin and Aβ fibrils reveal polymorphic remodeling in mixed amyloid systems.Nature communications · 2026Article
- Phagocytes as plaque catalysts: Human macrophages generate seeding-competent Aβ42 fibrils with cross-seeding activity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Naringenin as a dual-target modulator of RAGE-NF-κB signaling and Aβ fibrillization in Alzheimer's disease: integrated computational and experimental analyses.Frontiers in pharmacology · 2026Article
- Energetic profiling reveals thermodynamic principles underlying amyloid fibril maturation.Nature communications · 2025Article
- Phagocytes as Plaque Catalysts: Human Macrophages Actively Generate Pathogenic Aβ42 Fibrils with Seeding and Cross-Seeding Potency.bioRxiv : the preprint server for biology · 2025Article
- Human and Mouse Alzheimer's Seeds Differentially Affect Amyloid Deposition and Microglia-Dependent Plaque Response in Aged Mice.Aging cell · 2025Article
- Medin drives Aβ40 to adopt Aβ42-like fibril polymorphs in vitro.bioRxiv : the preprint server for biology · 2025Article
- Peptidomimetics Targeting the Amyloidogenicity of Nucleophosmin 1 Mutations in Acute Myeloid Leukemia.Chembiochem : a European journal of chemical biology · 2025Article
- Dual modulation of amyloid beta and tau aggregation and dissociation in Alzheimer's disease: a comprehensive review of the characteristics and therapeutic strategies.Translational neurodegeneration · 2025Review
- Heterotypic Interactions of Amyloid β and the Islet Amyloid Polypeptide Produce Mixed Aggregates with Non-Native Fibril Structure.The journal of physical chemistry letters · 2024Article
- Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting.Pharmacological reviews · 2024Review
- Heterotypic Seeding Generates Mixed Amyloid Polymorphs.Small science · 2024Article
- A core proteome profile unites mouse models and patients in Alzheimer disease.Cell reports. Medicine · 2024Article
- Heterotypic Seeding Generates Mixed Amyloid Polymorphs.bioRxiv : the preprint server for biology · 2024Article
- Mechanisms and pathology of protein misfolding and aggregation.Nature reviews. Molecular cell biology · 2023Review
- Identification of inflammasome signaling proteins in neurons and microglia in early and intermediate stages of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2023Article
- An Exploration of Multiple Component Peptide Assemblies by Enzyme-Instructed Self-Assembly.ChemSystemsChem · 2023Article
- Heterotypic Amyloid β interactions facilitate amyloid assembly and modify amyloid structure.The EMBO journal · 2022Article
- Insights into Network of Hot Spots of Aggregation in Nucleophosmin 1.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
It is still unclear why pathological amyloid deposition initiates in specific brain regions or why some cells or tissues are more susceptible than others. Amyloid deposition is determined by the self-assembly of short protein segments called aggregation-prone regions (APRs) that favour cross-β structure. Here, we investigated whether Aβ amyloid assembly can be modified by heterotypic interactions between Aβ APRs and short homologous segments in otherwise unrelated human proteins. Mining existing proteomics data of Aβ plaques from AD patients revealed an enrichment in proteins that harbour such homologous sequences to the Aβ APRs, suggesting heterotypic amyloid interactions may occur in patients. We identified homologous APRs from such proteins and show that they can modify Aβ assembly kinetics, fibril morphology and deposition pattern in vitro. Moreover, we found three of these proteins upon transient expression in an Aβ reporter cell line promote Aβ amyloid aggregation. Strikingly, we did not find a bias towards heterotypic interactions in plaques from AD mouse models where Aβ self-aggregation is observed. Based on these data, we propose that heterotypic APR interactions may play a hitherto unrealized role in amyloid-deposition diseases.
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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.