ReviewInternational journal of molecular sciences2020
The Toxicity and Polymorphism of β-Amyloid Oligomers.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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
85 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Salivary Biomarkers for Alzheimer's Disease: A Systematic Review with Meta-Analysis.International journal of molecular sciences · 2024Pooled it
- Safety, tolerability and immunogenicity of vaccine ALZ-101 in patients with early Alzheimer's disease: randomised, controlled trial.Alzheimer's research & therapy · 2026Trial
- Design of bifunctional pyridinophane ligands as MnInorganic chemistry frontiers · 2026Article
- Exposure to oligomeric and fibrillar species of amyloid-β induces toxicity and impairs extravillous trophoblast cell function in vitro.Placenta · 2026Article
- The concentric β-barrel hypothesis for amyloids: Models of soluble and transmembrane amyloid-β42 oligomers and channels composed of identical subunits and GM1 gangliosides.bioRxiv : the preprint server for biology · 2026Article
- Radiation-Induced Neurodegeneration.Biomedicines · 2026Review
- The diagnostic value of plasma Aβ42 and Aβ40 in Alzheimer's disease: current status, challenges, and impacting variables.Journal of neurology · 2025Review
- Identification of a glia-associated amyloid β oligomer subtype and the rescue from reactive astrogliosis by inhibitor NU-9.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Oral diseases as emerging risk factors for Alzheimer's disease: A scoping review.The Japanese dental science review · 2025Review
- Unravelling the myriad physiologic roles of transthyretin: critical considerations for treating transthyretin amyloidosis.Annals of medicine · 2025Review
- Presenilin Loss Impairs Synaptic Transmission and Causes Axonal Degeneration through Ryanodine Receptor Dysfunction, Independent of γ-Secretase Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Small-Molecule Inhibitors of Amyloid Beta: Insights from Molecular Dynamics-Part B: Natural Compounds.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Protein aggregation and neurodegenerative disease: Structural outlook for the novel therapeutics.Proteins · 2025Review
- Tinosinenside A inhibits neuroinflammation and protects HT22 cells by suppressing the TLR4/NF-κB/NLRP3 signaling pathway in BV2 cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Morphological and Molecular Profiling of Amyloid-β Species in Alzheimer's Pathogenesis.Molecular neurobiology · 2025Review
- Silibinin's role in counteracting neuronal apoptosis and synaptic dysfunction in Alzheimer's disease models.Apoptosis : an international journal on programmed cell death · 2025Article
- Small-Molecule Inhibitors of Amyloid Beta: Insights from Molecular Dynamics-Part A: Endogenous Compounds and Repurposed Drugs.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Microglial double stranded DNA accumulation induced by DNase II deficiency drives neuroinflammation and neurodegeneration.Journal of neuroinflammation · 2025Article
- Biophysical insights into the molecular mechanisms of beta amyloid aggregation and its toxic effects in Alzheimer's disease.Frontiers in molecular biosciences · 2025Review
- Neutrophils from Alzheimer's disease mice fail to phagocytose debris and show altered release of immune modulators with age.Frontiers in immunology · 2025Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
It is widely accepted that β-amyloid oligomers (Aβos) play a key role in the progression of Alzheimer's disease (AD) by inducing neuron damage and cognitive impairment, but Aβos are highly heterogeneous in their size, structure and cytotoxicity, making the corresponding studies tough to carry out. Nevertheless, a number of studies have recently made remarkable progress in the describing the characteristics and pathogenicity of Aβos. We here review the mechanisms by which Aβos exert their neuropathogenesis for AD progression, including receptor binding, cell membrane destruction, mitochondrial damage, Ca
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Identifiers
What Socratic holds
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 Socratic graph.