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@ARTICLE{Levin:163370,
      author       = {Levin, Johannes and Nübling, Georg and Giese, Armin and
                      Janzen, Annette and Oertel, Wolfgang H},
      title        = {{N}europrotektive {T}herapien bei idiopathischen,
                      genetischen und atypischen {P}arkinson-{S}yndromen mit
                      α-{S}ynuklein – {P}athologie.},
      journal      = {Der Nervenarzt},
      volume       = {92},
      number       = {12},
      issn         = {1433-0407},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2022-00133},
      pages        = {1249 - 1259},
      year         = {2021},
      abstract     = {The key aspect of the classification of neurodegenerative
                      diseases is the histopathological detection of certain
                      proteins in the brain. The various disease entities are
                      distinguished with respect to the type of detected protein
                      and with respect to the configuration and localization of
                      the corresponding protein aggregates. Aggregates of
                      alpha-synuclein (ASYN) are the defining hallmark of several
                      neurodegenerative disorders termed synucleinopathies. The
                      most well-known diseases in this spectrum are Parkinson's
                      disease (PD) with neuronal detection of Lewy bodies,
                      dementia with Lewy bodies (DLB), with additional detection
                      of beta-amyloid and multiple system atrophy (MSA), where
                      ASYN aggregates are found in glia cells in the form of
                      Papp-Lantos inclusions. ASYN has been identified as a key
                      target for the development of therapeutic approaches to
                      synucleinopathies given its central role in the
                      pathophysiology of these diseases. Current treatment
                      strategies can be roughly classified into six groups: 1)
                      lowering ASYN expression (antisense therapy), 2) inhibition
                      of formation of toxic ASYN aggregates (aggregation
                      inhibitors, chelators), 3) dissolving or removal of
                      intracellular or extracellular toxic AYSN aggregates (active
                      and passive immunotherapy, aggregation inhibitors), 4)
                      enhancement of cellular clearance mechanisms (autophagy,
                      lysosomal microphagy) for removal of toxic forms of
                      alpha-synuclein, 5) modulation of neuroinflammatory
                      processes and 6) neuroprotective strategies. This article
                      summarizes the current therapeutic approaches and sheds
                      light on promising future treatment approaches.},
      subtyp        = {Review Article},
      keywords     = {Humans / Neurodegenerative Diseases: diagnosis /
                      Neurodegenerative Diseases: genetics / Neurodegenerative
                      Diseases: therapy / Neurons / Parkinson Disease: diagnosis /
                      Parkinson Disease: genetics / Parkinson Disease: therapy /
                      Synucleinopathies / alpha-Synuclein: genetics /
                      Disease-modifying drugs (Other) / Lewy body dementia (Other)
                      / Multiple system atrophy (Other) / Parkinson’s disease
                      (Other) / Synucleinopathies (Other) / alpha-Synuclein (NLM
                      Chemicals)},
      cin          = {AG Levin},
      ddc          = {610},
      cid          = {I:(DE-2719)1111016},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34735584},
      pmc          = {pmc:PMC8648656},
      doi          = {10.1007/s00115-021-01220-y},
      url          = {https://pub.dzne.de/record/163370},
}