Parkin, a protein already linked to some cases of early-onset Parkinson’s disease, has been found to regulate how cells absorb and process dietary fats, according to research by the National Institutes of Health (NIH).
Parkinson’s typically affects people over 50, but is known to show in people in their 20s (about 5 to 10 percent of cases). This form of early-onset Parkinson’s affects actor, author, and Parkinson’s activist Michael J. Fox.
Parkin mutations are present in about 37 percent of individuals with early-onset Parkinson’s. However, in laboratory studies, mice with Parkin deformities did not show obvious symptoms of the disease. The preliminary study, published online in the Journal of Clinical Investigation, suggests that Parkin mutations may be an indirect contribution to some early-onset Parkinson’s cases by creating differences in the amount and types of fat in the body.
“This discovery shows that the clues to understand Parkinson’s disease may not necessarily be in the brain,” said study leader Michael Sack, M.D., chief of the Laboratory of Mitochondrial Biology in Cardiometabolic Syndromes at the NIH’s National Heart, Lung, and Blood Institute.
The research team, composed of scientists from the National Heart, Lung and Blood Institute (NHLBI) and the NIH’s National Institute of Neurological Disorders and Stroke, found that mice with mutated Parkin did not gain weight from a high-fat laboratory diet, as average mice typically do.
As scientists examined the organs of the Parkin-defective mice, they found that the cells had lower levels of certain proteins responsible for transporting fat. On the other hand, average mice who ate the same high-fat diet had high levels of these fat-carrying proteins, as well as high levels of Parkin, suggesting that Parkin is involved in the transportation of fats.
A similar pattern was found when researchers analyzed blood cells from patients enrolled in the NIH Parkinson’s Clinic. In lab tests, cells from people with Parkin mutations had more fat absorption problems. These results show that these findings could be applicable to humans.
Regarding fat and its relation to Parkinson’s, Sack notes that the destroyed brain cells are found in a region called the substantia nigra, which controls movement, among other roles. Sack and his team will continue to conduct early-stage clinical studies to test the link between fat metabolism and Parkinson’s.
“The neurons in this part of the brain are extremely active. Each one has over 300,000 connections and is continuously transmitting information,” said Sack.
“These neurons require good support in the form of their fat and cholesterol membrane. If the right types of fat aren’t available, then cell integrity will be sub-par and they could be prone to damage.”