Potential human transmission of amyloid beta pathology: surveillance and risks

Elsa Lauwers, Giovanna Lalli, Sebastian Brandner, John Collinge, Veerle Compernolle, Charles Duyckaerts, Gustaf Edgren, Stephane Haik, John Hardy, Adel Helmy, Adrian Ivinson, Zane Jaunmuktane, Mathias Jucker, Richard Knight, Robin Lemmens, Seth Love, Simon Mead, Bart de Strooper*

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)

Abstract

Studies in experimental animals show apparent transmissibility of amyloidogenic proteins associated with prion, Alzheimer’s, Parkinson’s or other neurodegenerative diseases. While these data raise potential concerns for public health, convincing evidence for human iatrogenic transmission currently only exists for prions and for β-amyloid (Aβ) after systemic injections of contaminated cadaver-derived growth hormone extracts or dura mater grafts. While these procedures are now obsolete, recent reports raise the possibility of iatrogenic Aβ transmission through putatively contaminated neurosurgical equipment. Iatrogenic Aβ-transmission appears to cause amyloid deposition in brain parenchyma and blood vessel walls, resulting in cerebral amyloid angiopathy (CAA) after several decades. CAA can cause life-threatening brain haemorrhages, yet there is currently no proof that Aβ-transmission could also lead to Alzheimer's dementia. Longer term, larger scale epidemiological studies and sensitive, cost-efficient amyloid detection tools are needed to better understand potential Aβ transmission routes and clarify whether other proteopathic seeds can be transferred iatrogenically.
Original languageEnglish
Pages (from-to)872-878
Number of pages7
JournalLancet Neurology
Volume19
Issue number10
Early online date16 Sep 2020
DOIs
Publication statusPublished - 1 Oct 2020

Keywords

  • Amyloid-beta
  • prion
  • proteopathic seed
  • iatrogenic transmission
  • neurosurgery
  • blood transfusion

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