This RNA buildup, which the researchers believe may be a marker of neurodegenerative diseases, can reduce protein production. The researchers observed this phenomenon in both mouse and human brains, especially in a part of the brain called the striatum — a site involved in diseases such as Parkinson’s and Huntington’s.
“The brain is very metabolically active, and over time, that causes oxidative damage, but it affects some neurons more than others,” says Christopher Burge, an MIT professor of biology. “This phenomenon appears to be a previously unrecognized consequence of oxidative stress, which impacts hundreds of genes and may influence translation and RNA regulation globally.”
Burge and Myriam Heiman, a member of the Picower Institute and the Latham Family Career Development Associate Professor of Brain and Cognitive Sciences, are the senior authors of the paper, which appears in the Nov. 27 issue of Cell Reports. Peter Sudmant, a former MIT postdoc, is the lead author of the paper, and Picower Institute postdoc Hyeseung Lee and former postdoc Daniel Dominguez are also authors.
Above: Neurons from mice aged 19 months (bottom row) show much higher rates of oxidative stress than neurons from 9-week-old mice (top row). Lipofuscin, a molecule associated with aging-related oxidative stress, appears red.