Investigating the Role of Free Radicals in Huntington's Disease Using Drosophila Melanogaster
Year: 2019
Type: article
Abstract: During normal cell metabolism, reactive oxygen species (ROS) are produced as a byproduct of oxidative phosphorylation. ROS are utilized in the cell as a signaling molecule and can be maintained at healthy levels by cellular antioxidants. However, when the cell experiences oxidative stress due to environmental or genetic conditions, levels of ROS can exceed healthy levels and inhibit necessary life functions by damaging biomolecules and cellular structures. This loss of function can lead to physiological decline and neurodegeneration, such as in diseases like Alzheimer’s, amyotrophic lateral sclerosis (ALS), and, potentially, Huntington’s disease. The following experiments use the model genetic organism Drosophila melanogaster to test whether ROS accumulation affects the symptoms of individuals infected with Huntington’s disease, compared with individuals fed a molecular antioxidant supplement, MitoQ. We found that while MitoQ was expected to alleviate symptoms of Huntington’s disease, individuals supplemented with MitoQ experienced delayed development and detrimental motor function across time independent of genotype or sex.
Source: Lincoln (University of Nebraska)
Author: Jennifer Libov
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
Funder: National Science Foundation
OpenAlex ID: W2940065896