Detecting Parkinson’s Disease Early
The genetic revolution of the 1990s has spurred the identification of seven disease-causing genes and many additional genes that constitute risk factors for Parkinson’s. Deciphering the function of these genes has facilitated our capacity to understand pathways involved in the disease process. Everyday there are breakthrough publications featured on Medical News Today, Viartis Parkinson’s Disease News and other search sites for Parkinson’s research.
The Parkinson Progressive Marker initiative (PPMI) developed by The Michael J. Fox Foundation has established early biological markers for Parkinson disease (PD). Studying families with an established genetic component to the disease increases our ability to find measureable indicators of early PD and, with that, a more accurate tool in the search for therapies to slow or stop the disease. A blood-based biomarker would, of course, be the least invasive, cost-effective type of marker.
On September 24, 2015, Viartis featured a project with great promise for providing that long sought after biomarker. Robert Nagele and his team at Durin Technologies and New Jersey’s Rowan-School of Osteopathic Medicine published in Immunology Letters the results of a study in which they screened early-stage Parkinson’s blood samples with microarrays containing thousands of autoantibodies.
In 2011 Nagele and his team had reported using autoantibody profiling and sophisticated analysis software to distinguished Alzheimer disease samples both from non-demented controls as well as from other non-neurological and neurological disorders, including Parkinson disease. In 2012, the team identified 10 out of a panel of thousands of autoantibodies that were capable of distinguishing PD samples from controls with 93% sensitivity and 100% specificity. In the current study, they have identified just four autoantibody biomarkers capable of distinguishing early Parkinson disease from those with mild to moderate Parkinson’s with an overall accuracy of 97%.
Antibodies are protective proteins that a person’s immune system builds to fight off what it recognizes as foreign or “non-self” (pollen, for instance). When the body somehow fails to recognize its own cells, tissues, and/or organs, autoantibodies build up that target “self.” Nagele’s rationale is illustrated in Fig. 3. of his paper: The body’s natural immune response to debris released by dying cells—even in early PD—is to produce autoantibodies. Then, as the disease pathology progresses, more abundant and complex disease-associated debris will alter the spectrum of autoantibodies produced.
Once again we see the power of an independent researcher able to fly with a vision that could very well revolutionize PD diagnosis and shorten the road on which we travel to find therapeutic interventions for Parkinson’s.
by Alice Lazzarini, PhD