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Related Experiment Video

Updated: Sep 20, 2025

Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans

Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans

Published on: January 8, 2015

Exogenous prion-like proteins and their potential to trigger cognitive dysfunction.

Jofre Seira Curto¹, Adan Dominguez Martinez^1,2, Genis Perez Collell¹

¹Unitat de Bioquímica, Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, Barcelona, Spain.

Molecular Systems Biology

|May 27, 2025

Summary

This summary is machine-generated.

Ingesting prion-like proteins from gut bacteria, like Helicobacter pylori, can impair memory and increase oxidative stress. This research highlights the gut microbiome as a source of such proteins, potentially impacting cognitive function.

Keywords:

Aggregation Amyloid Microbiome Neurodegeneration Prion Protein

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Last Updated: Sep 20, 2025

Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans

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Published on: January 8, 2015

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Protein Misfolding Cyclic Amplification of Prions

Protein Misfolding Cyclic Amplification of Prions

Published on: November 7, 2012

Area of Science:

Microbiology and Neuroscience
Protein Biochemistry
Gastroenterology

Background:

The gut microbiome produces proteins, including prion-like sequences, with largely unknown health implications.
Prion-like proteins can propagate across species, raising concerns about potential disease transmission and development.

Purpose of the Study:

To investigate the relationship between exogenous prion-like protein properties and their phenotypic effects after ingestion.
To explore the role of gut bacteria, particularly Helicobacter pylori, as a source of functional prion-like proteins.
To determine if ingested prion-like proteins can induce cognitive dysfunction and associated physiological changes.

Main Methods:

Computational analysis of gut bacterial proteomes to identify prion-like sequences.
Design and synthesis of prion-like sequences forming amyloid fibrils.
In vitro assays using yeast (Sup35 model) to assess prion propagation.
In vivo studies using Caenorhabditis elegans fed bacteria expressing prion-like proteins.

Main Results:

Enrichment of prion-like sequences identified in Helicobacter pylori.
Synthetic prion-like sequences formed amyloid fibrils, inhibited amyloid-beta aggregation, and propagated in yeast.
C. elegans fed bacteria with these proteins showed associative memory loss and increased lipid oxidation.

Conclusions:

Gut microbiota, especially H. pylori, serves as a reservoir for exogenous prion-like sequences.
The gut acts as an entry point for molecules that can trigger cognitive dysfunction.
A link exists between memory impairment, aggregate conformational state, and oxidative stress.