ReviewInternational journal of molecular sciences2018
Targeting Amyloid Aggregation: An Overview of Strategies and Mechanisms.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Impact of nanoparticles on amyloid β-induced Alzheimer's disease, tuberculosis, leprosy and cancer: a systematic review.Bioscience reports · 2023Pooled it
- Protein Recognition and Amyloid Remodeling Governed by Paddlewheel Diruthenium Coordination Chemistry.Inorganic chemistry · 2026Article
- Drug-Induced Reduction in 80Q Aggregates in aBiomedicines · 2026Article
- Covalent Modulation of Protein Misfolding and Aggregation Processes in the Context of Neurodegenerative Diseases.Archiv der Pharmazie · 2026Review
- Effects of acetylation on human insulin structure, and dynamics at different temperatures: A molecular dynamics simulation study.Journal of biosciences · 2026Article
- Low-Dimensional Nanomaterials in Alzheimer's Disease: Current Applications.Current Alzheimer research · 2026Review
- Neurodegeneration Through the Lens of Bioinformatics Approaches: Computational Mechanisms of Protein Misfolding.International journal of molecular sciences · 2025Review
- Article
- Senescent-like border-associated macrophages regulate cognitive aging via migrasome-mediated induction of paracrine senescence in microglia.Nature aging · 2025Article
- Article
- Acetylcholinesterase as a Multifunctional Target in Amyloid-Driven Neurodegeneration: From Dual-Site Inhibitors to Anti-Agregation Strategies.International journal of molecular sciences · 2025Review
- 2-Styrylquinolines with Push-Pull Architectures as Sensors for β-Amyloid Aggregation with Theranostic Properties.International journal of molecular sciences · 2025Article
- Targeted drug delivery in neurodegenerative diseases: the role of nanotechnology.Frontiers in medicine · 2025Review
- Modulation of Biological Membranes Using Small-Molecule Compounds to Counter Toxicity Caused by Amyloidogenic Proteins.Membranes · 2024Review
- Discovery of novel coumarin triazolyl and phenoxyphenyl triazolyl derivatives targeting amyloid beta aggregation-mediated oxidative stress and neuroinflammation for enhanced neuroprotection.RSC medicinal chemistry · 2024Article
- A Potent Sybody Selectively Inhibits α-Synuclein Amyloid Formation by Binding to the P1 Region.Journal of medicinal chemistry · 2024Article
- Can local heating and molecular crowders disintegrate amyloid aggregates?Chemical science · 2024Article
- Review
- Disaggregation of amyloid-beta fibrils via natural metabolites using long timescale replica exchange molecular dynamics simulation studies.Journal of molecular modeling · 2024Article
- Updating the Pharmacological Effects of α-Mangostin Compound and Unraveling Its Mechanism of Action: A Computational Study Review.Drug design, development and therapy · 2024Review
3 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
4 authors.
Funding
Abstract
Amyloids result from the aggregation of a set of diverse proteins, due to either specific mutations or promoting intra- or extra-cellular conditions. Structurally, they are rich in intermolecular β-sheets and are the causative agents of several diseases, both neurodegenerative and systemic. It is believed that the most toxic species are small aggregates, referred to as oligomers, rather than the final fibrillar assemblies. Their mechanisms of toxicity are mostly mediated by aberrant interactions with the cell membranes, with resulting derangement of membrane-related functions. Much effort is being exerted in the search for natural antiamyloid agents, and/or in the development of synthetic molecules. Actually, it is well documented that the prevention of amyloid aggregation results in several cytoprotective effects. Here, we portray the state of the art in the field. Several natural compounds are effective antiamyloid agents, notably tetracyclines and polyphenols. They are generally non-specific, as documented by their partially overlapping mechanisms and the capability to interfere with the aggregation of several unrelated proteins. Among rationally designed molecules, we mention the prominent examples of β-breakers peptides, whole antibodies and fragments thereof, and the special case of drugs with contrasting transthyretin aggregation. In this framework, we stress the pivotal role of the computational approaches. When combined with biophysical methods, in several cases they have helped clarify in detail the protein/drug modes of interaction, which makes it plausible that more effective drugs will be developed in the future.
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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.