ArticleFEBS letters2017
Amyloidogenicity and toxicity of the reverse and scrambled variants of amyloid-β 1-42.
Article in FEBS letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 52 citations in OpenAlex.
- YIAD-0501 directly dissociates aggregates of full-length and N-terminal pyroglutamate-modified forms of Aβ.Alzheimer's research & therapy · 2026Article
- Rationally Designed Pentapeptide Analogs of Aβ19-23 Fragment as Potent Inhibitors of Aβ42 Aggregation.Molecules (Basel, Switzerland) · 2025Article
- Unveiling the Interplay: Neurovascular Coupling, Astrocytes and G Protein-Coupled Receptors in Alzheimer's Disease.ACS pharmacology & translational science · 2025Review
- A subcellular sampling instrument allows spatial resolution of amyloid deposit-derived organelle-specific effects in microglia.Communications biology · 2025Article
- Adverse Effects of AβBiomolecules · 2024Article
- Ceftriaxone Modulates Ubiquitination of α-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid Receptors to Improve Long-Term Potentiation Impairment Induced by Exogenous β-Amyloid in a Glutamate Transporter-1 Dependent Manner.Molecular neurobiology · 2024Article
- TDP-43 Promotes Amyloid-Beta Toxicity by Delaying Fibril Maturation via Direct Molecular Interaction.ACS chemical neuroscience · 2024Article
- A Diruthenium Metallodrug as a Potent Inhibitor of Amyloid-β Aggregation: Synergism of Mechanisms of Action.Inorganic chemistry · 2024Article
- Neurodegeneration-related genes influencemicroPublication biology · 2024Article
- Disrupting Dimeric β-Amyloid by Electric Fields.ACS physical chemistry Au · 2023Article
- Dityrosine cross-linking and its potential roles in Alzheimer's disease.Frontiers in neuroscience · 2023Review
- The amyloid precursor protein: a converging point in Alzheimer's disease.Molecular neurobiology · 2022Review
- Potential Roles of α-amylase in Alzheimer's Disease: Biomarker and Drug Target.Current neuropharmacology · 2022Review
- Activation of PLCβ1 enhances endocannabinoid mobilization to restore hippocampal spike-timing-dependent potentiation and contextual fear memory impaired by Alzheimer's amyloidosis.Alzheimer's research & therapy · 2021Article
- An evaluation of the self-assembly enhancing properties of cell-derived hexameric amyloid-β.Scientific reports · 2021Article
- Outer-membrane-acting peptides and lipid II-targeting antibiotics cooperatively kill Gram-negative pathogens.Communications biology · 2021Article
- Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in aIBRO reports · 2020Article
- Ginsenoside Rg1 reduces β‑amyloid levels by inhibiting CDΚ5‑induced PPARγ phosphorylation in a neuron model of Alzheimer's disease.Molecular medicine reports · 2020Article
- Tryptophan-galactosylamine conjugates inhibit and disaggregate amyloid fibrils of Aβ42 and hIAPP peptides while reducing their toxicity.Communications biology · 2020Article
- Synthesis and biological activity study of the retro-isomer of RhTx against TRPV1.RSC advances · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
β-amyloid 1-42 (Aβ1-42) is a self-assembling peptide that goes through many conformational and morphological changes before forming the fibrils that are deposited in extracellular plaques characteristic of Alzheimer's disease. The link between Aβ1-42 structure and toxicity is of major interest, in particular, the neurotoxic potential of oligomeric species. Many studies utilise reversed (Aβ42-1) and scrambled (AβS) forms of amyloid-β as control peptides. Here, using circular dichroism, thioflavin T fluorescence and transmission electron microscopy, we reveal that both control peptides self-assemble to form fibres within 24 h. However, oligomeric Aβ reduces cell survival of hippocampal neurons, while Aβ42-1 and Aβs have reduced effect on cellular health, which may arise from their ability to assemble rapidly to form protofibrils and fibrils.
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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.