Abstract
Alzheimer's disease (AD) is a neurodegenerative disease linked to loss of cognitive and motor abilities. The neurodegeneration is thought to be caused, in part, by the accumulation of Aβ peptides in the brain. Currently, there is no cure for AD, and the available treatments are rather limited in scope. Most of them are aimed at treating the symptoms, not preventing or reversing the progression of the disease. Recent studies have suggested a therapeutic potential for cannabidiol (CBD), a component of the Cannabis sativa plant. Both, in vitro and in vivo studies have shown improvement in some of the physiological and cognitive signs of the disease, suggesting it may be a better therapeutic strategy compared to current treatments. Given CBD's therapeutic potential and the increase in availability of commercial over‐the‐counter CBD‐based oils, this study is aimed at assessing the therapeutic potential of these products using an invertebrate model of AD. To achieve our aim, we decided to use a transgenic Caenorhabditis elegans worm strain that expresses human Aβ in neurons (CL2355). This is an inducible strain that shows behavioral deficits that make it a suitable model for AD. Prior to treating the animals, a toxicity assay was performed with several concentrations of a commercially available CBD oil. Although more animals need to be tested, preliminary results showed no significant effect of the CBD oil on the worms' mortality. Once we determine the optimal concentration of CBD, Aβ expression will be induced in synchronized animals from the CL2355 strain by a temperature upshift. This will be followed by a 24‐hour exposure to the CBD oil or the vehicle. By the time the CBD exposure ends, the animals will be adults, and behavioral testing will be performed. Specifically, we will perform a thrashing and a short‐term associative learning assay to test for locomotor and memory deficits respectively. Results from this study will allow us to determine whether commercially‐available CBD oils can either prevent or alleviate some of the deficits associated with AD and will support the use of invertebrate models to further explore new possibilities for the development of therapeutic strategies for AD and other neurodegenerative disorders.Support or Funding InformationPUCPR‐PR Louis Stokes Alliances for Minority ParticipationThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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