Protein crucial in preventing Parkinson’s

By destroying bad mitochondria, Parkin protects cells

Tossing out the old batteries of brain cells might keep those cells strong, new research suggests.

A key player in this process is a protein called Parkin, which is made by the Park2 gene. Mutations in the gene can knock out production of the protein, resulting in early onset of Parkinson’s, a movement disorder brought on when brain cells that produce dopamine die. But until now, researchers did not know how the protein’s presence worked to prevent cells from being affected by the disease.

Now researchers at the National Institutes of Health report online November 24 in the Journal of Cell Biology that Parkin slates defective mitochondria for destruction while leaving healthy mitochondria untouched. Mitochondria are organelles within plant and animal cells that generate energy.

Removing damaged mitochondria might help cells maintain efficient energy production or prevent the buildup of toxic byproducts that might trigger a cell’s death.

“If you weed out all the bad apples in a barrel, the barrel stays fresh,” says Richard Youle, a cell biologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Md., who led the study.

Details of how Parkin targets broken-down mitochondria for removal aren’t yet clear, but Youle and his crew are trying to discover the molecular pathway that leads to mitochondrial demolition.

Tina Hesman Saey is the senior staff writer and reports on molecular biology. She has a Ph.D. in molecular genetics from Washington University in St. Louis and a master’s degree in science journalism from Boston University.

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