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News in Brief

PD Linked to Flawed Recycling in Cells

For years, scientists have tried to explain the loss of dopamine-producing neurons that is found in people who have Parkinson’s disease (PD).

In the January 2 online issue of The Journal of Clinical Investigation, Ana Maria Cuervo, M.D., Ph.D., and her colleagues at Albert Einstein College of Medicine of Yeshiva University, along with scientists from Columbia University, the University of Pennsylvania, and Harvard Medical School suggest an explanation.

The team reports that in people with Parkinson’s, neurons die because an important cellular process called cell-mediated autophagy — essentially a cell’s recycling system — does not function properly. Autophagy keeps aging cells healthy by filtering damaged molecules through the cell, thus avoiding any potentially harmful build-up. Dr. Cuervo traced the PD-related malfunction, in part, to the role of a protein known as alpha-synuclein, which had already been known to build up abnormally in the brains of people with PD.

Researchers found that in PD, when alpha-synuclein interacts with dopamine (a neurotransmitter), the alpha-synuclein gets ‘stuck’ in the cell-cleaning process. This malfunction leads to a harmful build-up of molecules and, in turn, to the death of cells, which then causes symptoms of PD.

Dr. Cuervo’s earlier studies focused on mutations of alpha-synuclein and how they disrupted the same cellular process. However, this research applied only to a small group of people who had a relatively rare genetic form of PD. Her new findings are much more compelling because they may apply to all people with PD. Additionally, the cellular glitch that Dr. Cuervo has found can be targeted by therapeutics in a number of ways, so her study opens the door for researchers to investigate new treatment options for Parkinson’s disease.

NSAIDs May Reduce Parkinson’s Risk

Researchers at the UCLA School of Public Health reported in the November 5 edition of Neurology that the use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, may reduce a person’s risk of Parkinson’s disease (PD).

Angelika Wahner, Ph.D., and her team studied the impact of NSAID use among 579 people, about one-half of whom had PD and one-half that did not.

Dr. Wahner’s team questioned participants about their use of both aspirin and non-aspirin NSAIDs (naproxen, ibuprofen), asking whether participants had taken either type of NSAIDs once a week or more for at least a month at any point in their lives.

Researchers defined regular users of NSAIDs as those who took two or more pills a week for at least a month, and classified people who fell below those standards as non-regular users.

The UCLA team found a mild protective effect against PD among the regular users of non-aspirin NSAIDs. A protective effect was also found among women who were regular users of aspirin NSAIDs, especially for those who reported two or more years of use. Dr. Wahner hypothesized that the gender difference may be attributed to dosage. She speculated that women are more likely to have taken aspirin in higher doses, perhaps for arthritis or headaches, while men may have taken it in lower doses for other conditions, such as heart problems.

Dr. Wahner’s results are interesting because they suggest that the role of inflammation — already linked to cell death in PD — needs to be further studied and could be an avenue for future treatments. However, the design of this study — a retrospective dietary survey which attempts to match people with PD and normal control subjects — cannot provide definitive information about the relationships between NSAIDs and PD. The relative risk of PD among people who are not taking NSAIDs was actually very slight, and the differences between groups could have occurred for unrelated reasons. Therefore, researchers are not yet recommending NSAIDs for prevention against PD. The area needs more investigation, both to clarify more specifically which NSAIDs may be protective and why a protective effect may exist.


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