Session: 668 Neurobiology and neuronal signaling I
(668.3) Effects of Cannabidiol in a Caenorhabditis Elegans Amyotrophic Lateral Sclerosis Model
Monday, April 4, 2022
12:30 PM – 1:45 PM
Location: Exhibit/Poster Hall A-B - Pennsylvania Convention Center
Poster Board Number: A345
Romola Cavet (The Nueva School), Juliet Sostena (The Nueva School), Albert Huang (The Nueva School), Paul Hauser (The Nueva School), Luke De (The Nueva School)
Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease caused by the progressive death of motor neurons. Cannabidiol, the second most prevalent cannabinoid in the Cannabis sativa plant, is a potential therapeutic tool for ALS due to its antioxidant, anti-inflammatory, and anti-spasticity effects, as well as its complementary role in treating other neurodegenerative diseases. In SOD1-G93A murine ALS models, cannabinoids have been shown to slow disease progression, extending lifespan and increasing motor function. However, the effects of specific cannabinoids—including cannabidiol—are yet undefined and their functions slowing disease progression are unknown. To advance this understanding we aim to study the effects of cannabidiol treatment in a Caenorhabditis elegans ALS model: a SOD-1 mutant transgenic strain with SOD-1 aggregation in muscular cells. We will use a death assay to measure the lifespan of SOD-1 mutant C. elegans and cannabidiol-treated SOD-1 mutant C. elegans to investigate whether treatment with cannabidiol impacts the lifespan of SOD-1 mutants. To assess mechanosensation, we will touch C. elegans with sutures of various sizes, based on the Von Frey filaments touch response assay in humans. We will develop a novel computational analysis system to measure C. elegans movement in response to touch. We will then compare the motor response of the SOD-1 mutant transgenic strain to wild type and study if cannabidiol modulates a possible change in motor response. This study will evaluate the functions of cannabidiol as a potential therapeutic tool in ALS using a SOD-1 mutant C. elegans model.
Support or Funding Information
Support for this research was provided by the Nueva School.
Support for this research was provided by the Nueva School.amp;nbsp;