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@ARTICLE{Lauwers:164429,
      author       = {Lauwers, Elsa and Lalli, Giovanna and Brandner, Sebastian
                      and Collinge, John and Compernolle, Veerle and Duyckaerts,
                      Charles and Edgren, Gustaf and Haïk, Stéphane and Hardy,
                      John and Helmy, Adel and Ivinson, Adrian J and Jaunmuktane,
                      Zane and Jucker, Mathias and Knight, Richard and Lemmens,
                      Robin and Lin, I-Chun and Love, Seth and Mead, Simon and
                      Perry, V Hugh and Pickett, James and Poppy, Guy and Radford,
                      Sheena E and Rousseau, Frederic and Routledge, Carol and
                      Schiavo, Giampietro and Schymkowitz, Joost and Selkoe,
                      Dennis J and Smith, Colin and Thal, Dietmar R and Theys, Tom
                      and Tiberghien, Pierre and van den Burg, Peter and
                      Vandekerckhove, Philippe and Walton, Clare and Zaaijer, Hans
                      L and Zetterberg, Henrik and De Strooper, Bart},
      title        = {{P}otential human transmission of amyloid β pathology:
                      surveillance and risks},
      journal      = {The lancet / Neurology},
      volume       = {19},
      number       = {10},
      issn         = {1474-4422},
      address      = {London},
      publisher    = {Lancet Publ. Group},
      reportid     = {DZNE-2022-00981},
      pages        = {872 - 878},
      year         = {2020},
      abstract     = {Studies in experimental animals show transmissibility of
                      amyloidogenic proteins associated with prion diseases,
                      Alzheimer's disease, Parkinson's disease, and other
                      neurodegenerative diseases. Although these data raise
                      potential concerns for public health, convincing evidence
                      for human iatrogenic transmission only exists for prions and
                      amyloid β after systemic injections of contaminated growth
                      hormone extracts or dura mater grafts derived from cadavers.
                      Even though these procedures are now obsolete, some reports
                      raise the possibility of iatrogenic transmission of amyloid
                      β through putatively contaminated neurosurgical equipment.
                      Iatrogenic transmission of amyloid β might lead to amyloid
                      deposition in the brain parenchyma and blood vessel walls,
                      potentially resulting in cerebral amyloid angiopathy after
                      several decades. Cerebral amyloid angiopathy can cause
                      life-threatening brain haemorrhages; yet, there is no proof
                      that the transmission of amyloid β can also lead to
                      Alzheimer's dementia. Large, long-term epidemiological
                      studies and sensitive, cost-efficient tools to detect
                      amyloid are needed to better understand any potential routes
                      of amyloid β transmission and to clarify whether other
                      similar proteopathic seeds, such as tau or α-synuclein, can
                      also be transferred iatrogenically.},
      subtyp        = {Review Article},
      keywords     = {Alzheimer Disease: etiology / Alzheimer Disease: metabolism
                      / Alzheimer Disease: pathology / Amyloid beta-Peptides:
                      metabolism / Amyloid beta-Peptides: toxicity / Animals /
                      Creutzfeldt-Jakob Syndrome: metabolism / Creutzfeldt-Jakob
                      Syndrome: pathology / Creutzfeldt-Jakob Syndrome:
                      transmission / Humans / Neurodegenerative Diseases: etiology
                      / Neurodegenerative Diseases: metabolism / Neurodegenerative
                      Diseases: pathology / Parkinson Disease: etiology /
                      Parkinson Disease: metabolism / Parkinson Disease: pathology
                      / Population Surveillance / Risk Factors},
      cin          = {AG Jucker},
      ddc          = {610},
      cid          = {I:(DE-2719)1210001},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32949547},
      doi          = {10.1016/S1474-4422(20)30238-6},
      url          = {https://pub.dzne.de/record/164429},
}