When telephone lines go down, or Internet connections are lost, our communities temporarily come to a halt. What if something similar were found to be happening in Parkinson's? This is the focus of Dr. Schmitz and her team at the PDF Research Center at Columbia University Medical Center.
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2010 Research Highlights
In 2010, PDF funded $5.5 million to support Parkinson's research. Here are some highlights:
- A New Strategy for Neuroprotection in Parkinson’s Disease
- Sleepless in the World of Parkinson’s Disease
- Scientists Discover Key Process that Contributes to Common Form of Parkinson’s
In a new analysis of current Parkinson’s research, Robert E. Burke, M.D., and his colleagues at Columbia University, with funding from a PDF center grant, found that only about 30 percent of a person’s dopamine neurons have died by the time that individual is diagnosed with the disease. These new findings contrast with a widely-cited number from previous studies that 50 percent or more of these cells have been lost at time of diagnosis.
The motor symptoms of Parkinson’s are thought to develop when dopamine neurons die, but in Dr. Burke’s report, which appeared in the June 2010 issue of Annals of Neurology, he and his colleagues argue that it is more than simply cell death the leads to the onset of PD. Instead, they point out, the development of Parkinson’s is also due to problems with communication which takes place through the cells’ axons. Much like telephones lines downed by a powerful storm, the researchers say that PD is a storm that disrupts the proper communication of dopamine in the brain, causing PD symptoms before nerve cells completely die.
The new hypothesis of Dr. Burke and his colleagues – that people newly diagnosed with PD may have many more dopamine neurons than previously thought – provides grounds for optimism that therapies aimed at protecting these cells can be effective for treating PD. They recommend a new emphasis on neurorestoration therapies which would protect neurons by improving the health of axons. Restoring the health of axons may alleviate motor symptoms, prevent cell death, and, the authors say, possibly slow PD progression. The PDF-supported scientists caution that the field of understanding mechanisms of axon regeneration and the potential for axon regrowth is in its early stages.
We may have a new understanding of sleep issues and Parkinson’s thanks to PDF-funded researcher, Aleksandar Videnovic, M.D., M.Sc., assistant professor in the Department of Neurology at Northwestern’s Feinberg School of Medicine. Dr. Videnovic is closing in on the end of his three-year term of the recipient of the PDF/American Academy of Neurology Foundation (AANF) Clinician-Scientist Development Award. He leaves us with new knowledge of a sleep disorder known as daytime somnolence (excessive sleepiness) and its relation to circadian rhythms.
Anyone with Parkinson’s who has struggled through the day on little or no rest knows that sleep disorders can be very disruptive to daily life. Circadian rhythms are regular changes in processes—biochemical, physiological and behavioral—in our bodies that control our biological clock. While it is known that disturbances in circadian rhythms can cause sleep disorders in the general population, they “had not been systematically studied in PD,” says Dr. Videnovic. His work since 2008 has involved testing the hypothesis that people with PD who experience excessive daytime sleepiness have a disruption in circadian rhythms. He has been studying patterns of sleeping and waking in people with Parkinson’s in an ongoing clinical trial and exploring treatments, such as light therapy, that correct imbalances in the body’s circadian rhythms. These treatments may be a more effective solution for sleep disorders than medicated sleep aids, which have proven ineffective in people with PD and have caused unpleasant side effects.
We look forward to seeing Dr. Videnovic’s results in 2011. As he tells us, the increased attention to sleep disorders will lead to the development of practical tools that could be used to treat and manage them, improving quality of life for people with Parkinson’s.
New research, led by Scott A. Small, M.D., a scientist supported through PDF’s center grant to Columbia University, identified a molecular pathway—the polyamine pathway—that may explain how Parkinson’s develops in people who have no family history of the disease.
Presented in the September issue of the prestigious journal Proceedings of the National Academy of Sciences, Dr. Small and his colleagues used a recently available technique called gene expression profiling to compare which genes were “switched” on or off in cells from two adjacent areas of the brain, one affected by PD, the other not. They found that a gene responsible for preventing the accumulation of a certain class of chemicals in the cell, called polyamines, was lower in those people who had PD compared to those who did not.
The finding of an association between high polyamine levels and PD—if confirmed—may have two potentially important clinical implications. Since polyamines can be measured in blood and in cerebral spinal fluid, they may be used in tests for early detection of PD or even for monitoring the effectiveness of future therapies. Currently, no such blood or spinal fluid tests are available. In addition, lowering polyamines levels in cells has been suggested by the authors as a novel approach to modifying PD. Further research is needed to determine whether reducing polyamines may in fact ease PD symptoms or slow disease progression.
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