ReviewSeminars in cell & developmental biology2011
Misfolded protein aggregates: mechanisms, structures and potential for disease transmission.
Review in Seminars in cell & developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 2 of them syntheses 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.
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Who cites it
119 citing papers in PubMed, 2 syntheses or guidelines pooled it, 243 citations in OpenAlex.
- Poloxamer 188 (P188), A Potential Polymeric Protective Agent for Central Nervous System Disorders: A Systematic Review.Current neuropharmacology · 2022Pooled it
- The Role of Protein Misfolding and Tau Oligomers (TauOs) in Alzheimer's Disease (AD).International journal of molecular sciences · 2019Pooled it
- Complexation of Hen Egg White Lysozyme With Bioactive Phenolic Acids: Molecular Insights Into the Binding Mechanisms and Inhibitory Effects Against Protein Aggregation.Chemphyschem : a European journal of chemical physics and physical chemistry · 2026Article
- A Real Time Quaking Induced Conversion (RT-QuIC) Assay for Detection of Misfolded Insulin Protein.bioRxiv : the preprint server for biology · 2026Article
- Peptide-based therapeutics in the management of Alzheimer's disease (AD) and their potential to develop novel strategies.Metabolic brain disease · 2026Review
- Unraveling C‑Peptide's Role in MIDY: A Structural Perspective.ACS omega · 2026Article
- Physiological responses to mask-associated COFrontiers in public health · 2026Review
- Urinary Congophilia in Pre-Eclampsia: A Potential Diagnostic Biomarker.Journal of pregnancy · 2026Review
- Inhibition of cytotoxic fibrillation of human insulin using silver nanoparticles capped by aqueous extract of Echium amoenum.Scientific reports · 2025Article
- Nanoplasmonic Infrared Microarray Sensor Enabling Structural Protein Biomarker-Based Drug Screening for Neurodegenerative Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Comparative Evaluation of Bovine- and Porcine-Deproteinized Grafts for Guided Bone Regeneration: An In Vivo Study.Bioengineering (Basel, Switzerland) · 2025Article
- Endocytic Pathways Unveil the Role of Syndecans in the Seeding and Spreading of Pathological Protein Aggregates: Insights into Neurodegenerative Disorders.International journal of molecular sciences · 2025Review
- Peripheral administration of blood from tau transgenic animals exacerbates brain tau-associated pathology.PloS one · 2025Article
- Premature aging and metabolic diseases: the impact of telomere attrition.Frontiers in aging · 2025Review
- Integrative single-cell and cell-free plasma RNA transcriptomics identifies biomarkers for early non-invasive AD screening.Frontiers in aging neuroscience · 2025Article
- Comprehensive structural and functional analyses of RAD50 nsSNPs: from prediction to impact assessment.Frontiers in bioinformatics · 2025Article
- Structural diversity of Alzheimer-related protein aggregations revealed using photothermal ratio-metric micro-spectroscopy.Biomedical optics express · 2024Article
- Degradation and/or Dissociation of Neurodegenerative Disease-Related Factor Amyloid-β by a Suspension Containing Calcium Hydrogen Carbonate Mesoscopic Crystals.International journal of molecular sciences · 2024Article
- Evaluation of Alpha-Synuclein and Tau Antiaggregation Activity of Urea and Thiourea-Based Small Molecules for Neurodegenerative Disease Therapeutics.ACS chemical neuroscience · 2024Article
- CaMKII suppresses proteotoxicity by phosphorylating BAG3 in response to proteasomal dysfunction.EMBO reports · 2024Article
59 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 at 1 institution in 1 country.
Funding
Abstract
Some of the most prevalent human degenerative diseases appear as a result of the misfolding and aggregation of proteins. Compelling evidence suggest that misfolded protein aggregates play an important role in cell dysfunction and tissue damage, leading to the disease. Prion protein (Prion diseases), amyloid-beta (Alzheimer's disease), alpha-synuclein (Parkinson's disease), Huntingtin (Huntington's disease), serum amyloid A (AA amyloidosis) and islet amyloid polypeptide (type 2 diabetes) are some of the proteins that trigger disease when they get misfolded. The recent understanding of the crucial role of misfolded proteins as well as the structural requirements and mechanism of protein misfolding have raised the possibility that these diseases may be transmissible by self-propagation of the protein misfolding process in a similar way as the infamous prions transmit prion diseases. Future research in this field should aim to clarify this possibility and translate the knowledge of the basic disease mechanisms into development of novel strategies for early diagnosis and efficient treatment.
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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.