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Ibuprofen Linked to Reduced Risk of Parkinson’s Disease

A Harvard Medical School study, authored by Xiang Gao, MD, and colleagues, concludes that the use of ibuprofen may be associated with a reduced link of Parkinson’s disease. The study will be presented in Toronto at the upcoming American Academy of Neurology meeting, April 10-17, 2010. A total of 136,474 individuals enrolled in the Nurses’ Health Study and the Health Professionals Follow-up Study were studied. None of them had Parkinson’s disease at the onset of the study.

In a 6-year follow-up, 293 individuals developed Parkinson’s disease. The analysis of this study group concluded that ibuprofen use was associated with a significantly lower risk of Parkinson’s disease (relative risk, 0.62). Individuals who took 3 or more tablets per week showed a 40% lower risk than those who did not take this OTC analgesic. Additionally, the use of aspirin, acetaminophen, and other nonsteroidal antiinflammatory drugs showed no effect on risk for Parkinson’s disease.

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Management Guidelines for Duchenne Muscular Dystrophy
Duchenne muscular dystrophy (DMD) affects 1 in 3600 to 6000 live male births, but until now there have not been any comprehensive clinical guidelines in place to provide patient assessment or treatment recommendations for the health care community. Now, new comprehensive guidelines have been issued in 2 parts to standardize care and offer a framework for a coordinated multidisciplinary approach to diagnosis and management of this disease. Part 1 appeared in the January issue of The Lancet Neurology, and part 2, which focuses on the implementation of multidisciplinary care for DMD patients, was published online in February 2010. The study authors note that a comprehensive management strategy can favorably alter the natural history of the disease as well as improve the function, quality of life, and longevity of the patient.

Both parts of the study are available, with subscription, on www.thelancet.com.


Low Serotonin Levels Linked to Cause for SIDS

New findings about sudden infant death syndrome (SIDS), reported in the February 3, 2010, issue of The Journal of the American Medical Association, have brought to light the significance of low serotonin levels in the brainstem of infants with SIDS. This condition is the leading cause of death for infants aged 1 to 12 months in the United States. Lead researcher Hannah Kinney, MD, of Children’s Hospital in Boston, has studied the brainstem, which is responsible for regulating an infant’s involuntary actions—such as breathing, blood pressure, and heart rate—during sleep.

The study measured the levels of serotonin and tryptophan hydroxylase, the enzyme that makes serotonin, in 35 infants with SIDS and in 2 control groups. The serotonin levels in the lower brainstem were 26% lower in the SIDS infants compared with the controls; the hydroxylase levels were 22% lower. An infant with low serotonin levels may never move while sleeping. One risk factor for SIDS already identified by medical experts is sleeping on the stomach. This new study brings a second possible risk factor for this syndrome to light, and additional research will help determine what causes low serotonin levels in infants.


New Studies on Huntington’s Disease Shed Light on Disease Onset
Two studies sponsored by the National Institute of Neurological Disorders and Strokes postulate that changes in protein chemistry play a role in Huntington’s disease (HD). Potential modifications of these changes through drug therapies open the doors to possible prevention of this disease. Leslie Thompson, PhD, University of California-Irvine, and researchers discovered that the protein huntingtin—which causes HD in mutations— is phosphorylated by the inflammatory kinase IKK, enhancing its normal clearance. The process of phosphorylation of disease protein plays an important role in the disease’s pathogenesis. The California-Irvine study showed that the phosphorylation of serines 13 and 16 can regulate the clearance of huntingtin protein.

A related study led by researcher X. William Yang, MD, PhD, University of California-Los Angeles, revealed the same 2 serines played a critical role in huntingtin-induced disease pathogenesis. That study was published in the December 24 issue of Neuron. The National Institutes of Health issued a statement on both studies that discussed the new light shed on the biochemistry of the mutant huntingtin protein and pointed to potential targets for drug therapy. ■



FAST FACT: Parkinson’s disease affects an estimated 1 million individuals in the United States.