Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

HSV-1 reactivation as an emergent property of neuronal stress: implications for traumatic brain injury.

Journal of neuroinflammation·2026

Same author

Dogcatcher2: Improved statistical detection of transcriptional readthrough and repetitive element analysis across sequencing platforms.

bioRxiv : the preprint server for biology·2026

Same author

Multielectrode array characterization of human induced pluripotent stem cell derived neurons in co-culture with primary human astrocytes.

PloS one·2024

Same author

Multielectrode array characterization of human induced pluripotent stem cell derived neurons in co-culture with primary human astrocytes.

bioRxiv : the preprint server for biology·2024

Same author

The reverse transcriptase inhibitor 3TC protects against age-related cognitive dysfunction.

Aging cell·2023

Same author

TDP-43 knockdown in mouse model of ALS leads to dsRNA deposition, gliosis, and neurodegeneration in the spinal cord.

Cerebral cortex (New York, N.Y. : 1991)·2022

Search research articles

Related Experiment Video

Updated: Jun 7, 2026

Assaying β-amyloid Toxicity using a Transgenic C. elegans Model

Assaying β-amyloid Toxicity using a Transgenic C. elegans Model

Published on: October 9, 2010

Assaying β-amyloid toxicity using a transgenic C. elegans model.

Vishantie Dostal¹, Christopher D Link

¹Institute for Behavioral Genetics, University of Colorado, USA.

Journal of Visualized Experiments : Jove

|October 26, 2010

Summary

This summary is machine-generated.

This study details a protocol for measuring paralysis in transgenic worms expressing amyloid-beta (Aβ) to understand Alzheimer's disease mechanisms. This model allows researchers to quantify Aβ toxicity and test potential therapeutic interventions.

More Related Videos

A Caenorhabditis elegans Model System for Amylopathy Study

A Caenorhabditis elegans Model System for Amylopathy Study

Published on: May 17, 2013

Automated Behavioral Analysis of Large C. elegans Populations Using a Wide Field-of-view Tracking Platform

Automated Behavioral Analysis of Large C. elegans Populations Using a Wide Field-of-view Tracking Platform

Published on: November 28, 2018

Related Experiment Videos

Last Updated: Jun 7, 2026

Assaying β-amyloid Toxicity using a Transgenic C. elegans Model

Assaying β-amyloid Toxicity using a Transgenic C. elegans Model

Published on: October 9, 2010

A Caenorhabditis elegans Model System for Amylopathy Study

A Caenorhabditis elegans Model System for Amylopathy Study

Published on: May 17, 2013

Automated Behavioral Analysis of Large C. elegans Populations Using a Wide Field-of-view Tracking Platform

Automated Behavioral Analysis of Large C. elegans Populations Using a Wide Field-of-view Tracking Platform

Published on: November 28, 2018

Area of Science:

Neuroscience
Genetics
Molecular Biology

Background:

Amyloid-beta (Aβ) peptide accumulation is implicated in Alzheimer's disease pathogenesis.
Aβ also deposits in Inclusion Body Myositis, a human myopathy.
The nematode worm Caenorhabditis elegans serves as a model for studying Aβ toxicity.

Purpose of the Study:

To describe a protocol for measuring paralysis in a transgenic C. elegans model of Aβ toxicity.
To highlight experimental variables affecting paralysis measurements.
To facilitate research into Alzheimer's disease and related myopathies.

Main Methods:

Utilizing a transgenic C. elegans strain with temperature-inducible muscle expression of human Aβ.
Inducing paralysis by temperature upshift.
Quantifying the rate of paralysis as a measure of Aβ toxicity.

Main Results:

The described protocol allows for reproducible measurement of paralysis in response to Aβ expression.
Experimental variables influencing paralysis rate were identified.
This model system has been used to assess the efficacy of protective transgenes and Ginkgo biloba extracts.

Conclusions:

The C. elegans paralysis model provides a valuable tool for studying Aβ toxicity mechanisms.
This protocol enables the assessment of potential therapeutic interventions against Aβ-induced damage.
Further research using this model can elucidate pathways involved in neurodegenerative diseases.