ArticlePloS one2015
Structure-Based Peptide Design to Modulate Amyloid Beta Aggregation and Reduce Cytotoxicity.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed.
- Design and Verification Process of a Structure-Altering Peptide as a Microtubule Allosteric Polypeptide Against Cancer.The protein journal · 2025Article
- An 11-mer Synthetic Peptide Suppressing Aggregation of Aβ25-35 and Resolving Its Aggregated Form Improves Test Performance in an Aβ25-35-Induced Alzheimer's Mouse Model.Biomolecules · 2024Article
- Repurposing Anidulafungin for Alzheimer's Disease via Fragment-Based Drug Discovery.ACS chemical neuroscience · 2024Article
- A Snake Venom Peptide and Its Derivatives Prevent AβACS chemical neuroscience · 2024Article
- Amyloid Beta Leads to Decreased Acetylcholine Levels and Non-Small Cell Lung Cancer Cell Survival via a Mechanism That Involves p38 Mitogen-Activated Protein Kinase and Protein Kinase C in a p53-Dependent and -Independent Manner.International journal of molecular sciences · 2024Article
- Five-mer peptides prevent short-term spatial memory deficits in Aβ25-35-induced Alzheimer's model mouse by suppressing Aβ25-35 aggregation and resolving its aggregate form.Alzheimer's research & therapy · 2023Article
- Structure-Activity Relationship of 5-mer Catalytides, GSGYR and RYGSG.Biomolecules · 2022Article
- Computational screening for new neuroprotective ingredients against Alzheimer's disease from bilberry by cheminformatics approaches.Frontiers in nutrition · 2022Article
- Direct Delivery of ANA-TA9, a Peptide Capable of Aβ Hydrolysis, to the Brain by Intranasal Administration.Pharmaceutics · 2021Article
- Racemization in Post-Translational Modifications Relevance to Protein Aging, Aggregation and Neurodegeneration: Tip of the Iceberg.Symmetry · 2021Article
- Site-specific single point mutation by anthranilic acid in hIAPPRSC chemical biology · 2021Article
- Amyloid beta cleavage by ANA-TA9, a synthetic peptide from the ANA/BTG3 Box A region.Alzheimer's & dementia (New York, N. Y.) · 2021Article
- Arginine and Arginine-Rich Peptides as Modulators of Protein Aggregation and Cytotoxicity Associated With Alzheimer's Disease.Frontiers in molecular neuroscience · 2021Review
- How Does the Mono-Triazole Derivative Modulate AβACS omega · 2020Article
- Humanin Blocks the Aggregation of Amyloid-β Induced by Acetylcholinesterase, an Effect Abolished in the Presence of IGFBP-3.Biochemistry · 2020Article
- The Impact of Natural Compounds on S-Shaped Aβ42 Fibril: From Molecular Docking to Biophysical Characterization.International journal of molecular sciences · 2020Article
- Nanostructures Formed by Custom-Made Peptides Based on Amyloid Peptide Sequences and Their Inhibition by 2-Hydroxynaphthoquinone.Frontiers in chemistry · 2020Article
- Carotenoids as Novel Therapeutic Molecules Against Neurodegenerative Disorders: Chemistry and Molecular Docking Analysis.International journal of molecular sciences · 2019Review
- Catalytides derived from the Box A region in the ANA/BTG3 protein cleave amyloid-β fragment peptide.Heliyon · 2019Article
- Using chirality to probe the conformational dynamics and assembly of intrinsically disordered amyloid proteins.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The deposition of Aβ peptide in the brain is the key event in Alzheimer disease progression. Therefore, the prevention of Aβ self assembly into disease-associated oligomers is a logical strategy for treatment. π stacking is known to provide structural stability to many amyloids; two phenylalanine residues within the Aβ 14-23 self recognition element are in such an arrangement in many solved structures. Therefore, we targeted this structural stacking by substituting these two phenylalanine residues with their D-enantiomers. The resulting peptides were able to modulate Aβ aggregation in vitro and reduce Aβ cytotoxicity in primary neuronal cultures. Using kinetic analysis of fibril formation, electron microscopy and dynamic light scattering characterization of oligomer size distributions, we demonstrate that, in addition to altering fibril structural characteristics, these peptides can induce the formation of larger amorphous aggregates which are protective against toxic oligomers, possibly because they are able to sequester the toxic oligomers during co-incubation. Alternatively, they may alter the surface structure of the oligomers such that they can no longer interact with cells to induce toxic pathways.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.