A recent study states that a protein called alpha-synuclein linked to Parkinson’s disease adversely affects mitochondria and helps in the advancement of the disease
The researchers from the University of Buffalo, who have conducted the study titled ‘Differential mitochondrial roles for alpha-synuclein in DRP1-dependent fission and PINK1/Parkin-mediated oxidation’ believe that their findings will help in the development of drugs for Parkinson’s disease, a disorder of the central nervous system that hampers movement, and is characterised by tremors.
The study was conducted on fruit fly larvae, genetically made to produce remarkably high amounts of alpha-synuclein. “When fruit fly larvae expressed alpha-synuclein at elevated levels similar to what is seen in Parkinson’s disease, many of the mitochondria we observed became unhealthy, and many became fragmented,” explained one of the researchers, Shermali Gunawardena, in an article published on the website of University of Buffalo.
” Through detailed experiments, we also showed that different parts of the alpha-synuclein protein seem to be responsible for these two problems and that fragmented mitochondria can actually be healthy. This is a key finding because before, people thought fragmented mitochondria were unhealthy mitochondria,” added Gunawardena, PhD, associate professor of biological sciences in the University at Buffalo College of Arts and Sciences.
The study was published in the journal Cell Death and Disease. According to an article published in Drug Target Review, “Alpha-synuclein is a soluble, natively unfolded cytosolic protein that becomes structured when bound to phospholipids. Although the protein lacks an actual mitochondrial localisation sequence, previous studies suggest that alpha-synuclein contains a cryptic mitochondrial targeting sequence that can facilitate anchoring alpha-synuclein to mitochondrial membranes.”
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