A new study from researchers at Florida Atlantic University (FAU) is reportedly the first to show the Parkin gene — associated with developing early-onset Parkinson's disease — is turned on when cells are exposed to environmental insults that cause free radical formation and cataract formation.
For their study, the research team engineered eye lens cells to make them either normal Parkin or a mutant form of Parkin, and looked at whether Parkin function was required for lens cell mitochondrial function and lens cell survival. Not only did they find the Parkin gene is turned on when the cells are exposed to environmental insults, the researchers also discovered when mitochondria damaged by these environmental insults were removed, Parkin prevented free radical formation in lens cells and increased the cells' abilities to survive exposure to conditions that are associated with aging and the development of many degenerative diseases.
This data reportedly suggests an important function for Parkin in promoting the survival of not only lens cells, but many cells in the body. Additionally, researchers believe activation of the Parkin gene could prevent cell damage associated with age-related cataract formation.
The study was recently published in the journal Biochemica et Biophysica Acta: Molecular Basis of Disease.
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Source: Florida Atlantic University