ArticleScientific reports2016
Exposure to bacterial endotoxin generates a distinct strain of α-synuclein fibril.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 133 citations in OpenAlex.
- Review
- Prebiotics attenuate depressive-like behavior, neuroinflammation and synaptic plasticity in Parkinson's disease by modulating butyrate-producing gut bacteria.Inflammopharmacology · 2026Article
- Gut Dysbiosis and Microbiota-Derived Metabolites in Neurodegenerative Diseases: Molecular and Biochemical Mechanisms Along the Gut-Brain Axis.Molecules (Basel, Switzerland) · 2026Review
- Hidden faces of alpha-synuclein: Cryo-EM revelation of fibril polymorphs driven by disease, mutations, and PTMs.BBA advances · 2026Review
- Differential microglial responses to structurally distinct alpha-synuclein polymorphs.Molecular brain · 2025Article
- Article
- Dynein-Dependent Endo-Lysosomal Degradation Drives Lewy Body Disorders Accompanied by Aβ Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- α-Synuclein Pathology in Synucleinopathies: Mechanisms, Biomarkers, and Therapeutic Challenges.International journal of molecular sciences · 2025Review
- Olfactory Dysfunction as a Clinical Marker of Early Glymphatic Failure in Neurodegenerative Diseases.Diagnostics (Basel, Switzerland) · 2025Review
- Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances.Signal transduction and targeted therapy · 2025Review
- Review
- The role of vagus nerve stimulation in modulating Parkinson's disease via the microbiota-gut-brain axis: a comprehensive review.Frontiers in neurology · 2025Review
- Sulfate reducing bacteria induce α-synuclein in intestinal and neuronal cells and tissues and inhibit tyrosine hydroxylase in neuronal cells.Frontiers in neuroscience · 2025Article
- Parkinson's disease beyond the brain: implications for treatments.Frontiers in aging neuroscience · 2025Review
- In cell NMR reveals cells selectively amplify and structurally remodel amyloid fibrils.bioRxiv : the preprint server for biology · 2024Article
- The menace within: bacterial amyloids as a trigger for autoimmune and neurodegenerative diseases.Current opinion in microbiology · 2024Review
- Environmental risk factors provoke new thinking for prevention and treatment of dementia with Lewy bodies.Heliyon · 2024Review
- Mechanisms and pathology of protein misfolding and aggregation.Nature reviews. Molecular cell biology · 2023Review
- α-Synuclein oligomers and fibrils: partners in crime in synucleinopathies.Neural regeneration research · 2023Article
- Gut microbiome and Parkinson's disease: Perspective on pathogenesis and treatment.Journal of advanced research · 2023Review
25 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
A single amyloidogenic protein is implicated in multiple neurological diseases and capable of generating a number of aggregate "strains" with distinct structures. Among the amyloidogenic proteins, α-synuclein generates multiple patterns of proteinopathies in a group of diseases, such as Parkinson disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). However, the link between specific conformations and distinct pathologies, the key concept of the strain hypothesis, remains elusive. Here we show that in the presence of bacterial endotoxin, lipopolysaccharide (LPS), α-synuclein generated a self-renewable, structurally distinct fibril strain that consistently induced specific patterns of synucleinopathies in mice. These results suggest that amyloid fibrils with self-renewable structures cause distinct types of proteinopathies despite the identical primary structure and that exposure to exogenous pathogens may contribute to the diversity of synucleinopathies.
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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.