Parkinson's disease (PD) is recognized as a systemic condition, with clinical features potentially modifiable by dietary intervention. Diets high in saturated fats and refined sugars significantly increase PD risk and exacerbate motor and non-motor symptoms, yet precise metabolic mechanisms are unclear. To investigate the interplay between diet and PD, we used a model of early-onset PD under chronic glycative stress induced by prolonged high-fat high-sucrose (HFHS) diet. We found this obesogenic diet drives loss of fat and muscle mass in early-onset PD mice, with a selective vulnerability of glycolytic myofibers. We show that PD mice and early-onset familial PD patients are under pervasive glycative stress with pathological accumulation of advanced glycation end products (AGEs), including two previously unknown glycerinyl-AGE markers.
FörderungenStichting Parkinson Fonds Munich Graduate School of Systemic Neurosciences Munich Center for Systems Neurology Deutsches Zentrum fur Diabetesforschung ExNet-0041-Phase2-3 through the Initiative and Network Fund of the Helmholtz Association (SyNergy-HMGU)