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@ARTICLE{Szeg:278657,
      author       = {Szegő, Éva M and Höfs, Lennart and Antoniou, Anna and
                      Dinter, Elisabeth and Bernhardt, Nadine and Schneider, Anja
                      and Di Monte, Donato A and Falkenburger, Björn},
      title        = {{I}ntermittent fasting reduces alpha-synuclein pathology
                      and functional decline in a mouse model of {P}arkinson's
                      disease.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2025-00613},
      pages        = {4470},
      year         = {2025},
      abstract     = {Parkinson's disease (PD) is a neurodegenerative disorder
                      characterized by dopaminergic neuron degeneration and
                      α-synuclein (aSyn) accumulation. Environmental factors play
                      a significant role in PD progression, highlighting the
                      potential of non-pharmacological interventions. This study
                      investigates the therapeutic effects of intermittent fasting
                      (IF) in an rAAV-aSyn mouse model of PD. IF, initiated four
                      weeks post-induction of aSyn pathology, improved motor
                      function and reduced dopaminergic neuron and axon terminal
                      degeneration. Additionally, IF preserved dopamine levels and
                      synaptic integrity in the striatum. Mechanistically, IF
                      enhanced autophagic activity, promoting phosphorylated-aSyn
                      clearance and reducing its accumulation in insoluble brain
                      fractions. Transcriptome analysis revealed IF-induced
                      modulation of inflammation-related genes and microglial
                      activation. Validation in primary cultures confirmed that
                      autophagy activation and inflammatory modulators (CCL17,
                      IL-36RN) mitigate aSyn pathology. These findings suggest
                      that IF exerts neuroprotective effects, supporting further
                      exploration of IF and IF-mimicking therapies as potential PD
                      treatments.},
      keywords     = {Animals / alpha-Synuclein: metabolism / alpha-Synuclein:
                      genetics / Parkinson Disease: metabolism / Parkinson
                      Disease: pathology / Parkinson Disease: therapy / Parkinson
                      Disease: genetics / Fasting: physiology / Disease Models,
                      Animal / Mice / Dopaminergic Neurons: metabolism /
                      Dopaminergic Neurons: pathology / Male / Autophagy / Mice,
                      Inbred C57BL / Dopamine: metabolism / Humans / Corpus
                      Striatum: metabolism / Corpus Striatum: pathology /
                      Microglia: metabolism / Intermittent Fasting /
                      alpha-Synuclein (NLM Chemicals) / Dopamine (NLM Chemicals)},
      cin          = {AG Falkenburger / AG Di Monte / AG Schneider},
      ddc          = {500},
      cid          = {I:(DE-2719)1710012 / I:(DE-2719)1013008 /
                      I:(DE-2719)1011305},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40368903},
      doi          = {10.1038/s41467-025-59249-5},
      url          = {https://pub.dzne.de/record/278657},
}