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@ARTICLE{Woerman:905615,
      author       = {Woerman, Amanda L. and Tamgüney, Gültekin},
      title        = {{B}ody-first {P}arkinson’s disease and variant
                      {C}reutzfeldt–{J}akob disease – similar or different?},
      journal      = {Neurobiology of disease},
      volume       = {164},
      issn         = {0969-9961},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {FZJ-2022-00847},
      pages        = {105625},
      year         = {2022},
      abstract     = {In several neurodegenerative disorders, proteins that
                      typically exhibit an α-helical structure misfold into an
                      amyloid conformation rich in β-sheet content. Through a
                      self-templating mechanism, these amyloids are able to induce
                      additional protein misfolding, facilitating their
                      propagation throughout the central nervous system. This
                      disease mechanism was originally identified for the prion
                      protein (PrP), which misfolds into PrPSc in a number of
                      disorders, including variant Creutzfeldt–Jakob disease
                      (vCJD) and bovine spongiform encephalopathy (BSE). More
                      recently, the prion mechanism of disease was expanded to
                      include other proteins that rely on this self-templating
                      mechanism to cause progressive degeneration, including
                      α-synuclein misfolding in Parkinson’s disease (PD).
                      Several studies now suggest that PD patients can be
                      subcategorized based on where in the body misfolded
                      α-synuclein originates, either the brain or the gut,
                      similar to patients developing sporadic CJD or vCJD. In this
                      review, we discuss the human and animal model data
                      indicating that α-synuclein and PrPSc misfolding originates
                      in the gut in body-first PD and vCJD, and summarize the data
                      identifying the role of the autonomic nervous system in the
                      gut-brain axis of both diseases.},
      cin          = {IBI-7},
      ddc          = {570},
      cid          = {I:(DE-Juel1)IBI-7-20200312},
      pnm          = {5244 - Information Processing in Neuronal Networks
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35026401},
      UT           = {WOS:000782610700002},
      doi          = {10.1016/j.nbd.2022.105625},
      url          = {https://juser.fz-juelich.de/record/905615},
}