ReviewAnnals of Indian Academy of Neurology
Toxic species in amyloid disorders: Oligomers or mature fibrils.
Review in Annals of Indian Academy of Neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.
What it found
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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
108 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
- Natural Compounds for Alzheimer's Disease Therapy: A Systematic Review of Preclinical and Clinical Studies.International journal of molecular sciences · 2019Pooled it
- Amyloid-beta fibrils as active contributors to synaptic dysfunction in Alzheimer's disease.Acta pharmacologica Sinica · 2026Article
- Exposure to oligomeric and fibrillar species of amyloid-β induces toxicity and impairs extravillous trophoblast cell function in vitro.Placenta · 2026Article
- Spontaneous aging of mature amyloids alters structural stability, cytotoxicity, and susceptibility to biological clearance.Cell death discovery · 2026Article
- PARylation in Parkinson's disease: a bridge between Lewy body formation and neuronal cell death.Cell death & disease · 2026Article
- Helix-Aggregation Interplay in Nucleophosmin 1: Structural, Morphological, and Cytotoxic Consequences of Fragment Length.ACS omega · 2026Article
- Glycation at the Crossroads of Disease Pathogenesis: Mechanistic Insights and Therapeutic Frontiers.Diseases (Basel, Switzerland) · 2026Review
- Microfluidic platform for understanding Parkinson's disease and α-synuclein conformation.Translational neurodegeneration · 2025Review
- Epigallocatechin-3-Gallate: A potential amyloid Fibril Disaggregator of Serum amyloid A1.Biochemistry and biophysics reports · 2025Article
- Inorganic Polyphosphate: An Emerging Regulator of Neuronal Bioenergetics and Its Implications in Neuroprotection.Biomolecules · 2025Review
- Protective Effect of a Hexapeptide Derived from Rotifer-Specific SCO-Spondin Against Beta-Amyloid Toxicity.International journal of molecular sciences · 2025Article
- Particulate matter and co-occurring genetic risk induce oxidative stress and cardiac and brain Alzheimer's pathology.Communications biology · 2025Article
- The Promising Role of Selenium and Yeast in the Fight Against Protein Amyloidosis.Biological trace element research · 2025Review
- Neuroprotective Effects of Dehydroepiandrosterone Sulphate Against Aβ Toxicity and Accumulation in Cellular and Animal Model of Alzheimer's Disease.Biomedicines · 2025Article
- Multimer Detection System: A Universal Assay System for Differentiating Protein Oligomers from Monomers.International journal of molecular sciences · 2025Review
- Repurposing doxycycline for Alzheimer's treatment: Challenges from a nano-based drug delivery perspective.Brain, behavior, & immunity - health · 2024Article
- Alzheimer's Disease Immunotherapy and Mimetic Peptide Design for Drug Development: Mutation Screening, Molecular Dynamics, and a Quantum Biochemistry Approach Focusing on Aducanumab::Aβ2-7 Binding Affinity.ACS chemical neuroscience · 2024Article
- Modulation of Alzheimer's Disease Aβ40 Fibril Polymorphism by the Small Heat Shock Protein αB-Crystallin.Journal of the American Chemical Society · 2024Article
- Evaluating p-tau217 and p-tau231 as Biomarkers for Early Diagnosis and Differentiation of Alzheimer's Disease: A Narrative Review.Biomedicines · 2024Review
- Protein Misfolding in Pregnancy: Current Insights, Potential Mechanisms, and Implications for the Pathogenesis of Preeclampsia.Molecules (Basel, Switzerland) · 2024Review
48 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
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein aggregation is the hallmark of several neurodegenerative disorders. These protein aggregation (fibrillization) disorders are also known as amyloid disorders. The mechanism of protein aggregation involves conformation switch of the native protein, oligomer formation leading to protofibrils and finally mature fibrils. Mature fibrils have long been considered as the cause of disease pathogenesis; however, recent evidences suggest oligomeric intermediates formed during fibrillization to be toxic. In this review, we have tried to address the ongoing debate for these toxic amyloid species. We did an extensive literature search and collated information from Pubmed (http://www.ncbi.nlm.nih.gov) and Google search using various permutations and combinations of the following keywords: Neurodegeneration, amyloid disorders, protein aggregation, fibrils, oligomers, toxicity, Alzheimer's Disease, Parkinson's Disease. We describe different instances showing the toxicity of mature fibrils as well as oligomers in Alzheimer's Disease and Parkinson's Disease. Distinct structural framework and morphology of amyloid oligomers suggests difference in toxic effect between oligomers and fibrils. We highlight the difference in structure and proposed toxicity pathways for fibrils and oligomers. We also highlight the evidences indicating that intermediary oligomeric species can act as potential diagnostic biomarker. Since the formation of these toxic species follow a common structural switch among various amyloid disorders, the protein aggregation events can be targeted for developing broad-range therapeutics. The therapeutic trials based on the understanding of different protein conformers (monomers, oligomers, protofibrils and fibrils) in amyloid cascade are also described.
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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.