BUCK INSTITUTE FOR RESEARCH ON AGINGCellular senescence, the process by which cells cease to divide in response to stress, may be a double-edged sword. In addition to being an important anti-cancer mechanism, recent studies show it may also contribute to age-related tissue damage and inflammation. A study published in Cell Reports yesterday (January 23) suggests that cellular senescence could be a factor underlying neurodegeneration in sporadic forms of Parkinson’s disease.
“I think the proposition that cellular senescence drives neurodegeneration in Parkinson’s disease and other ageing-related neurodegenerative diseases . . . has a great deal of merit,” writes D James Surmeier, a physiologist at Northwestern University, to The Scientist in an email. “To my knowledge, [this study] is the first strong piece of evidence for this model.”
Cellular senescence may be the basis by which the herbicide and neurotoxin paraquat, which has been previously linked to Parkinson’s disease, can contribute to the disease, the researchers propose.
The vast majority of Parkinson’s disease cases are sporadic, rather than inherited, and caused by a combination of environmental and genetic factors. Julie Andersen, a neuroscientist at the Buck Institute for Research on Aging, says her laboratory decided to focus ...
