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@ARTICLE{Soto:276802,
      author       = {Soto, Claudio and Mollenhauer, Brit and Hansson, Oskar and
                      Kang, Un Jung and Alcalay, Roy N and Standaert, David and
                      Trenkwalder, Claudia and Marek, Kenneth and Galasko, Douglas
                      and Poston, Kathleen},
      title        = {{T}oward a biological definition of neuronal and glial
                      synucleinopathies.},
      journal      = {Nature medicine},
      volume       = {31},
      number       = {2},
      issn         = {1078-8956},
      address      = {[New York, NY]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2025-00327},
      pages        = {396 - 408},
      year         = {2025},
      abstract     = {Cerebral accumulation of alpha-synuclein (αSyn) aggregates
                      is the hallmark event in a group of neurodegenerative
                      diseases-collectively called synucleinopathies-which include
                      Parkinson's disease, dementia with Lewy bodies and multiple
                      system atrophy. Currently, these are diagnosed by their
                      clinical symptoms and definitively confirmed postmortem by
                      the presence of αSyn deposits in the brain. Here, we
                      summarize the drawbacks of the current clinical definition
                      of synucleinopathies and outline the rationale for moving
                      toward an earlier, biology-anchored definition of these
                      disorders, with or without the presence of clinical
                      symptoms. We underscore the utility of the αSyn seed
                      amplification assay to detect aggregated αSyn in living
                      patients and to differentiate between neuronal or glial
                      αSyn pathology. We anticipate that a biological definition
                      of synucleinopathies, if well-integrated with the current
                      clinical classifications, will enable further understanding
                      of the disease pathogenesis and contribute to the
                      development of effective, disease-modifying therapies.},
      subtyp        = {Review Article},
      keywords     = {Humans / Neuroglia: pathology / Neuroglia: metabolism /
                      alpha-Synuclein: metabolism / alpha-Synuclein: genetics /
                      Synucleinopathies: pathology / Synucleinopathies: metabolism
                      / Neurons: pathology / Neurons: metabolism / Parkinson
                      Disease: pathology / Parkinson Disease: genetics / Parkinson
                      Disease: metabolism / Brain: pathology / Brain: metabolism /
                      Multiple System Atrophy: pathology / Multiple System
                      Atrophy: metabolism / Multiple System Atrophy: genetics /
                      Lewy Body Disease: pathology / Lewy Body Disease: metabolism
                      / Lewy Body Disease: genetics / alpha-Synuclein (NLM
                      Chemicals)},
      cin          = {AG Fischer},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39885358},
      doi          = {10.1038/s41591-024-03469-7},
      url          = {https://pub.dzne.de/record/276802},
}