ReviewNature communications2025
Emerging biophysical origins and pathogenic implications of amyloid oligomers.
Review in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed.
- Zinc Fingers as Programmable Metalloprotein Scaffolds for Altering Pathogenic Biomolecular Phase Transitions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Temperature-Dependent Dynamics of Aβ42 and α-Synuclein Monomers and Early Oligomerization of Aβ42: Shared Residues Mediate Intra- and Intermolecular β-Sheets.ACS chemical neuroscience · 2026Article
- Pathogenic landscape shaped by cerebral amyloid oligomers.Neural regeneration research · 2026Article
- Degradation reshapes the toxic identity of polylactic acid microplastics through MSR1-dependent immune decoding in mouse kidney.Particle and fibre toxicology · 2026Article
- Tracking Protein Misfolding and Oligomerization: A Temperature-Controlled Ion Mobility-Mass Spectrometry Approach.Analytical chemistry · 2026Article
- Nanoplastics and Neurodegeneration: A Roadmap From Mechanism to Causation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- In vitro, cellular and in vivo studies of amyloid oligomers structure and toxicity: Challenges and advances.Protein science : a publication of the Protein Society · 2026Review
- Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026Review
- Physiological Functions of Side-Chain-Retaining Sterols in the Brain and Their Roles in Neurodegenerative Diseases.Metabolites · 2026Review
- A global thermodynamic-kinetic model capturing the hallmarks of liquid-liquid phase separation and amyloid aggregation.Cell reports. Physical science · 2026Article
- Exploring the gut-brain axis: dietary influences on Alzheimer's disease pathogenesis.Frontiers in microbiomes · 2026Review
- Retinal pigment epithelium pathology in age-related macular degeneration: mitigation with melatonin.Frontiers in medicine · 2026Review
- Amyloid β Peptide Modifies Membrane Architecture and Surface Electrostatic Properties of Human Red Blood Cells.International journal of molecular sciences · 2025Article
- Cerebral to Systemic Representations of Alzheimer's Pathogenesis Stimulated by Polystyrene Nanoplastics.Environment & health (Washington, D.C.) · 2025Article
- Mitochondrial Calcium Channels and MAM Interaction in Calcium Homeostasis Dysregulation in Parkinson's Disease.Neurochemical research · 2025Review
- The Evolution of Functional Amyloids and Their Impact on Host-Microbe Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Conformational Ensemble Dynamics of Intrinsically Disordered Full-Length α- and β-Synuclein Monomers.Journal of chemical information and modeling · 2025Article
- Aortic Stiffness and Alzheimer's Disease: The Medin Connection.Biomolecules · 2025Review
- Emergence of Compact Oligomers inside the Small-World Network of TDP-43 Condensates.The journal of physical chemistry letters · 2025Article
- Inhibitory mechanisms of amentoflavone on amyloid-β peptide aggregation revealed by replica exchange molecular dynamics.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The amyloid hypothesis has been a leading narrative concerning the pathophysiological foundation of Alzheimer's and Parkinson's disease. At the two ends of the hypothesis lie the functional protein monomers and the pathology-defining amyloid fibrils, while the early stages of protein aggregation are populated by polymorphic, transient and neurotoxic oligomers. As the structure and activity of oligomers are intertwined, here we show oligomers arising from liquid-liquid phase separation and β-barrel formation, their routes to neurodegeneration, and their role in cerebrovascular perturbation. Together, this Perspective converges on the multifaceted oligomer-axis central to the pathological origin and, hence, the treatment of amyloid 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.