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@ARTICLE{deMello:279047,
      author       = {de Mello, Natalia Prudente and Berger, Michelle Tamara and
                      Lagerborg, Kim A and Yan, Yingfei and Wettmarshausen,
                      Jennifer and Keipert, Susanne and Weidner, Leopold and
                      Tokarz, Janina and Möller, Gabriele and Ciciliot, Stefano
                      and Walia, Safal and Cheng, Yiming and Chudenkova, Margarita
                      and Artati, Anna and Weisenhorn, Daniela Vogt and Wurst,
                      Wolfgang and Adamski, Jerzy and Nilsson, Roland and Cossu,
                      Giovanni and Boon, Agnita and Kievit, Anneke and
                      Mandemakers, Wim and Bonifati, Vincenzo and Jain, Mohit and
                      Jastroch, Martin and Schmitt-Kopplin, Philippe and Perocchi,
                      Fabiana and Dyar, Kenneth Allen},
      title        = {{P}ervasive glycative stress links metabolic imbalance and
                      muscle atrophy in early-onset {P}arkinson's disease.},
      journal      = {Molecular metabolism},
      volume       = {97},
      issn         = {2212-8778},
      address      = {Oxford [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2025-00677},
      pages        = {102163},
      year         = {2025},
      abstract     = {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. Our objective here was to
                      investigate the interplay between diet and PD-associated
                      phenotypes from a metabolic perspective.We explored PARK7 KO
                      mice under chronic glycative stress induced by prolonged
                      high-fat high-sucrose (HFHS) diet. We investigated metabolic
                      consequences by combining classical metabolic phenotyping
                      (body composition, glucose tolerance, indirect calorimetry,
                      functional assays of isolated mitochondria) with
                      metabolomics profiling of biospecimens from mice and PD
                      patients.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
                      N-α-glycerinylarginine (α-GR) and N-α-glycerinyllysine
                      (α-GK), two previously unknown glycerinyl-AGE markers.Our
                      results offer the first proof for a direct link between
                      diet, accumulation of AGEs and genetics of PD. We also
                      expand the repertoire of clinically-relevant glycative
                      stress biomarkers to potentially define at-risk patients
                      before neurological or metabolic symptoms arise, and/or to
                      monitor disease onset, progression, and effects of
                      interventions.},
      keywords     = {Animals / Mice / Parkinson Disease: metabolism / Humans /
                      Male / Diet, High-Fat: adverse effects / Muscular Atrophy:
                      metabolism / Mice, Knockout / Glycation End Products,
                      Advanced: metabolism / Female / Mice, Inbred C57BL /
                      Metabolomics: methods / Muscle, Skeletal: metabolism /
                      Disease Models, Animal / Advanced glycation endproducts
                      (AGEs) (Other) / Biomarkers (Other) / Glycative stress
                      (Other) / Glycobiology (Other) / Muscle atrophy (Other) /
                      Parkinson's disease (Other) / Glycation End Products,
                      Advanced (NLM Chemicals)},
      cin          = {AG Wurst},
      ddc          = {610},
      cid          = {I:(DE-2719)1140001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40345387},
      doi          = {10.1016/j.molmet.2025.102163},
      url          = {https://pub.dzne.de/record/279047},
}