Could medications for high cholesterol protect against Parkinson disease (PD)?

Identifying patterns that are associated with Parkinson’s across large groups of patients—the study of epidemiology—can be confounded by many things. Health care systems in other countries like the single-payer, compulsory National Health Insurance program (NHI) implemented in Taiwan in 1995, provide a level of uniform data than is difficult to achieve in our country. A recent publication from Taiwan takes advantage of their NHI, in which over 98% of the population is enrolled, in order to shed light on the basic mechanisms of PD, and in turn on potential treatment. Parkinson’s and other neurodegenerative diseases have been thought to involve a cascade of inflammation in the brain so that inhibiting the inflammatory response may be a viable approach to therapy. Since the statin drugs that are used to treat elevated cholesterol have anti-inflammatory effects, and they have been shown to reduce alpha-synuclein aggregation in animal models, a Taiwanese team studied whether various statins could affect the risk for developing PD—i.e. could the statins be protective? Other such studies to date, using self-reporting and without the numbers of patients needed to separate out (control for) the effect of most factors that could skew the results, have been inconsistent. Lee, et al (Neurology, July 30, 2013) were able to collect information on the effect of discontinuing different statins while controlling for the accuracy of diagnosis and the co-occurrence of other diseases and drugs. They compared one class of lipophilic (fat-loving) statins to the class of hydrophilic (water-loving) statins. A significant protective effect was demonstrated only by the continued use of the lipophilic statins. Because these cross the blood-brain barrier more readily, and because the disease process starts long before symptoms appear, the authors postulate that a protective effect of lipophilic statins may exist at the level of the dopamine brain receptors rather than on the degeneration of dopamine neurons.

  • Should you switch to a llipophilic statin?
  • Should you self-administer statin-like drugs?
  • Would I be better off if I also had high cholesterol requiring that I take statins?

Of Course Not!

What we can take from this comprehensive study is the knowledge that competent researchers are chipping away at the mechanism by which cells die, and each piece that is added to the puzzle exposes a different view of the overall picture which will one day be revealed to us. KTF

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