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Glucose metabolism in the brain as a biomarker for idiopathic REM sleep behaviour disorder
Description
Parkinson's disease is typically diagnosed only after the onset of motor symptoms. However, by this stage, a significant number of dopamine-producing nerve cells in the midbrain have already been lost. Consequently, potential treatments designed to protect these nerve cells intervene too late, meaning that current treatments can only address the symptoms of the disease.
Non-motor symptoms can manifest years or even decades earlier. One of the earliest is idiopathic REM sleep behavior disorder (iRBD), where individuals physically act out their dreams during sleep. Given that people with iRBD have a substantially elevated risk of subsequently developing Parkinson's disease, they represent a crucial target population for identifying biomarkers that could facilitate earlier diagnosis and treatment.
Previous research by our group has demonstrated that Parkinson's patients exhibit reduced glucose metabolism in the midbrain, which may indicate neuronal loss in this region. Therefore, one objective of the present study is to determine whether this metabolic alteration is already observable in individuals with iRBD. The second objective addresses why motor symptoms only emerge after a substantial proportion of dopamine-producing nerve cells have been lost. This suggests the brain employs compensatory mechanisms to counteract the effects of dopamine depletion. Such mechanisms may help explain the considerable variability in symptoms and disease progression among patients. A deeper understanding of these compensatory mechanisms could not only enhance the prediction of individual disease trajectories but also open new avenues for future therapeutic strategies. In this study, these mechanisms will be investigated using neuroimaging techniques and clinical assessments.
Contact
Mrs. Anneke Below und Frau Dr. rer. nat Marina Ruppert-Junck
Telefon: 06421/58 - 65299
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