Dietary iron imbalances either way spell trouble for healthy cells, triggering a chain of cellular events in the brain that increases the odds of developing Parkinson's disease, a degenerative condition affecting movement and balance in more than 1 million Americans each year. But excessive iron levels are worse -- much worse.
The findings from a study by Florida State University scientist Cathy Levenson are described in "The Role of Dietary Iron Restrictions in a Mouse Model of Parkinson's Disease" and will appear in an upcoming edition of Experimental Neurology. Levenson is an associate professor of nutrition, food and exercise sciences in FSU's College of Human Sciences and a faculty member in both the Program in Neuroscience and graduate program in molecular biophysics.
"We define our work here at the cellular level," said Levenson from her laboratory at FSU's Biomedical Research Facility. "Our primary research objective is to better understand how trace metal imbalances, which are associated with neuropsychiatric and neurodegenerative diseases, affect the molecular mechanisms that regulate gene expression."
Levenson performed the mouse model portion of the study in collaboration with Mark Mattson, Laboratory of Neurosciences chief at the National Institute on Aging in Bethesda, Md. Mice were fed varying amounts of iron to determine levels that precipitated onset or hastened the progression of Parkinson's-like symptoms such as tremors and balance problems, both in healthy rodents and where risk factors existed.
High levels of iron caused Parkinson's-like symptoms even in healthy mice without apparent risk factors for the illness, while accelerating the decline and death of those already diagnosed with the disease.