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.
POF Topic(s)30201 - Metabolic Health 30202 - Environmental Health 30505 - New Technologies for Biomedical Discoveries 30204 - Cell Programming and Repair
Forschungsfeld(er)Helmholtz Diabetes Center Environmental Sciences Enabling and Novel Technologies Genetics and Epidemiology
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)