Biomarkers for PD: How can we approach complexity?

By the time patients present with motor symptoms of Parkinson disease (PD), two-thirds of their dopaminergic neurons will have died and at least some of the remaining dopaminergic neurons may already be affected by the molecular mechanisms that will eventually lead to their death. It is plausible to assume that any neuroprotective therapy for PD might be much more effective if individuals at risk could be started on such therapy while they are still in the premotor stage of the disease. Excellent epidemiologic combined with long-time clinical follow-up studies have unequivocally established that individuals with common but nonspecific symptoms, such as autonomic dysfunction including constipation, erectile and urinary dysfunction, and neuropsychiatric symptoms like depression or hyposmia, are at increased risk of developing PD.¹ Other premotor manifestations of PD, in particular REM sleep behavioral disorder (RBD), are much more characteristic for premotor PD, but comparatively rare. Any attempt to base the identification of premotor PD on clinical observation only is therefore limited by low specificity (as would be the case for constipation) or sensitivity (as for RBD). Moreover, low specificity of some markers alludes to another major drawback in the search of biomarkers: the heterogeneity of PD. To evaluate markers reliably, it is therefore important to assess cohorts in whom homogenous pathogenesis can be assumed. This is the case in individuals who share the same genetically determined risk. Monogenetic forms of PD are, however, rare, and it is therefore difficult to recruit such genetically determined cohorts.

http://www.neurology.org/cgi/content/short/80/7/608?rss=1

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Júlio Leonardo B. Pereira

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