Journal Article (Review Article) DZNE-2022-00981

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Potential human transmission of amyloid β pathology: surveillance and risks

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2020
Lancet Publ. Group London

The lancet <London> / Neurology 19(10), 872 - 878 () [10.1016/S1474-4422(20)30238-6]

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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.

Keyword(s): Alzheimer Disease: etiology (MeSH) ; Alzheimer Disease: metabolism (MeSH) ; Alzheimer Disease: pathology (MeSH) ; Amyloid beta-Peptides: metabolism (MeSH) ; Amyloid beta-Peptides: toxicity (MeSH) ; Animals (MeSH) ; Creutzfeldt-Jakob Syndrome: metabolism (MeSH) ; Creutzfeldt-Jakob Syndrome: pathology (MeSH) ; Creutzfeldt-Jakob Syndrome: transmission (MeSH) ; Humans (MeSH) ; Neurodegenerative Diseases: etiology (MeSH) ; Neurodegenerative Diseases: metabolism (MeSH) ; Neurodegenerative Diseases: pathology (MeSH) ; Parkinson Disease: etiology (MeSH) ; Parkinson Disease: metabolism (MeSH) ; Parkinson Disease: pathology (MeSH) ; Population Surveillance (MeSH) ; Risk Factors (MeSH)

Classification:

Contributing Institute(s):
  1. Cell Biology of Neurological Diseases (AG Jucker)
Research Program(s):
  1. 899 - ohne Topic (POF4-899) (POF4-899)

Appears in the scientific report 2020
Database coverage:
Medline ; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 50 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection
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 Record created 2022-05-31, last modified 2024-06-17


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