The Roots of Compulsion
Surveys have found that up to 14% of PD patients treated with dopamine agonist medication exhibit signs of compulsive gambling, shopping, eating, and sexual behavior. In the January 8, 2013 edition of Neurology, Daniel Weintraub et al looked to see if recently diagnosed untreated PD patients displayed similar signs of so-called impulse control disorders (ICDs), when compared to healthy controls. They didn’t. Looks like the drugs are to blame.
Two small studies seeking diagnostic biomarkers for PD claim some success. The Mayo Clinic’s Charles Adler will present results of the diagnostic value of salivary gland proteins at the American Academy of Neurology’s 65th Annual Meeting in San Diego, March 16 to 23, 2013. Additionally, Sok Kean Khoo et al of the Center for Neurodegenerative Science and Genomic Microarray Core Facility at the Van Andel Institute, Grand Rapids, Michigan, reported in the December 2012 edition of JPD on their continuing efforts to detect PD-specific miRNAs in plasma.
The January 21, 2013 on-line edition of Movement Disorders includes a report by Wills et al about the potential anti-dyskinetic properties of coffee. Numerous epidemiological studies have previously demonstrated that people who drink a lot of coffee are less likely than average to develop Parkinson’s disease. This study tried to find out if coffee had therapeutic benefits as well. The Mass General Hospital led team report that PD patients who consumed more than 12 ounces of coffee a day (that’s one tall Starbucks) developed dyskinesias at about two thirds (61%) the rate of PD patients who consumed less than four ounces a day.
There are good theoretical reasons for taking this finding seriously. It turns out that caffeine wakes us up in the morning by blocking adenosine receptors, like the A2a receptor subtype found extensively in the striatum. Caffeine, a so-called A2a antagonist, also blocks a principal dopamine receptor (D2), which in PD patients is overactive (in the basal ganglia’s “indirect pathway”). More than a decade or so ago, such factors inspired pharmaceutical companies to search for other A2a antagonists as potential agents to stop the bad learning and thereby mitigate levodopa-induced dyskinesia and on/off fluctuations.
Will such drugs make much of a difference? The jury is still out. After early success, Istradefylline (Kyowa Pharmaceutical, Inc.) failed to beat a placebo in its phase III trial. Preladenant (Schering-Plough ) is currently in phase III testing for both early stage and advanced PD. Another A2a antagonist, Tozadenant (Biote) is in early clinical testing.
In the meantime, whether or not you have PD, a daily cup coffee won’t do you any harm and might do you some good.