Tiny changes in DNA that have been linked to Parkinson’s, the second most common neurodegenerative disorder after Alzheimer’s, can be found not only in brain cells, where they are expected, but also in liver, fat, immune and developmental cells, says a study. These findings may one day contribute to the development of preventative interventions before the disease’s effects become pronounced.
“When we looked at the data, we were quite surprised to see the variation in tissue types,” said Gerry Coetzee, the study’s corresponding author and professor at Van Andel Research Institute (VARI)in Grand Rapids in Michigan, US.”Ultimately, if we can more precisely define risk factors for Parkinson’s, we can develop ways to mitigate them early on. We still have a long way to go but these findings are some of the first steps down that path,” said Coetzee.
Although these DNA changes, called single-nucleotide polymorphisms (SNPs), are very small, an accumulation of enough SNPs can significantly heighten a person’s risk of developing Parkinson’s.
While scientists know that five to 10 per cent of Parkinson’s cases are passed down genetically through families, they are still determining what’s behind the majority of cases.
The prevailing theory is a mix of genetic and environmental factors create a perfect storm, leading to the hallmark clumping of abnormal proteins that spread through the brain, killing cells that produce a chemical called dopamine that is vital for voluntary movement.
Using information from Roadmap Epigenomics Mapping Consortium as a guide, Coetzee and other researchers analysed 21 of these risk areas, called loci, in 77 cell types.
Of these, the team found 12 loci across several tissue types that were particularly enriched–or full of SNPS – indicating an increase in risk.