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Acta Neuropathol. 2018 May;135(5):671-679. doi: 10.1007/s00401-018-1822-2. Epub 2018 Feb 15.

Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery.

Author information

1
Division of Neuropathology, The National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London, WC1N 3BG, UK.
2
Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK.
3
Portuguese Brain Bank, Neuropathology Unit, Department of Neuroscience, Centro Hospitalar Universitario do Porto, 4099-001, Porto, Portugal.
4
Department of Neurology, Hospital Egas Moniz, Centro Hospitalar de Lisboa Ocidental, 1449-005, Lisbon, Portugal.
5
Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK.
6
Department of Imaging and Pathology, University of Leuven, 3000, Louvain, Belgium.
7
Medical Research Council Prion Unit at UCL, UCL Institute of Prion Diseases, Queen Square, London, WC1N 3BG, UK.
8
National Prion Clinic, National Hospital for Neurology and Neurosurgery, UCL Hospitals NHS Foundation Trust, Queen Square, London, WC1N 3BG, UK.
9
Division of Neuropathology, The National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London, WC1N 3BG, UK. s.brandner@ucl.ac.uk.
10
Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK. s.brandner@ucl.ac.uk.

Abstract

Amyloid-β (Aβ) is a peptide deposited in the brain parenchyma in Alzheimer's disease and in cerebral blood vessels, causing cerebral amyloid angiopathy (CAA). Aβ pathology is transmissible experimentally in animals and through medical procedures in humans, such as contaminated growth hormone or dura mater transplantation in the context of iatrogenic prion disease. Here, we present four patients who underwent neurosurgical procedures during childhood or teenage years and presented with intracerebral haemorrhage approximately three decades later, caused by severe CAA. None of these patients carried pathogenic mutations associated with early Aβ pathology development. In addition, we identified in the literature four patients with a history of neurosurgical intervention and subsequent development of CAA. These findings raise the possibility that Aβ pathology may be transmissible, as prion disease is, through neurosurgical procedures.

KEYWORDS:

Amyloid-β; Aβ; CAA; Cerebral amyloid angiopathy; Decontamination; Head trauma; Intracerebral haemorrhage; Neurosurgery; Prion diseases; Proteopathic seeding; TBI; Transmission; Traumatic brain injury

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