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- Lauwers, E. (author)
Potential human transmission of amyloid beta pathology: surveillance and risks
- Article/chapterEnglish2020
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- 2020
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- LIBRIS-ID:oai:gup.ub.gu.se/299758
- https://gup.ub.gu.se/publication/299758URI
- https://doi.org/10.1016/S1474-4422(20)30238-6DOI
- http://kipublications.ki.se/Default.aspx?queryparsed=id:144971374URI
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- Language:English
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- 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 beta 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 beta through putatively contaminated neurosurgical equipment. Iatrogenic transmission of amyloid beta 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 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 beta transmission and to clarify whether other similar proteopathic seeds, such as tau or alpha-synuclein, can also be transferred iatrogenically.
Subject headings and genre
- MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin hsv//swe
- MEDICAL AND HEALTH SCIENCES Clinical Medicine hsv//eng
- CREUTZFELDT-JAKOB-DISEASE; DURA-MATER; BLOOD-TRANSFUSION; GROWTH-HORMONE; PRION; ANGIOPATHY; PROTEIN; NEURODEGENERATION; ASSOCIATION; ALZHEIMERS
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- Lalli, G. (author)
- Brandner, S. (author)
- Collinge, J. (author)
- Compernolle, V. (author)
- Duyckaerts, C. (author)
- Edgren, G.Karolinska Institutet (author)
- Haik, S. (author)
- Hardy, J. (author)
- Helmy, A. (author)
- Ivinson, A. J. (author)
- Jaunmuktane, Z. (author)
- Jucker, M. (author)
- Knight, R. (author)
- Lemmens, R. (author)
- Lin, I. C. (author)
- Love, S. (author)
- Mead, S. (author)
- Perry, V. H. (author)
- Pickett, J. (author)
- Poppy, G. (author)
- Radford, S. E. (author)
- Rousseau, F. (author)
- Routledge, C. (author)
- Schiavo, G. (author)
- Schymkowitz, J. (author)
- Selkoe, D. J. (author)
- Smith, C. (author)
- Thal, D. R. (author)
- Theys, T. (author)
- Tiberghien, P. (author)
- van den Burg, P. (author)
- Vandekerckhove, P. (author)
- Walton, C. (author)
- Zaaijer, H. L. (author)
- Zetterberg, Henrik,1973Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xzethe (author)
- De Strooper, B. (author)
- Karolinska InstitutetInstitutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi (creator_code:org_t)
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- In:Lancet Neurology19:10, s. 872-8781474-44221474-4465
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- Edgren, G.
- Haik, S.
- Hardy, J.
- Helmy, A.
- Ivinson, A. J.
- Jaunmuktane, Z.
- Jucker, M.
- Knight, R.
- Lemmens, R.
- Lin, I. C.
- Love, S.
- Mead, S.
- Perry, V. H.
- Pickett, J.
- Poppy, G.
- Radford, S. E.
- Rousseau, F.
- Routledge, C.
- Schiavo, G.
- Schymkowitz, J.
- Selkoe, D. J.
- Smith, C.
- Thal, D. R.
- Theys, T.
- Tiberghien, P.
- van den Burg, P.
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