ReviewActa neuropathologica2014
Is there a risk of prion-like disease transmission by Alzheimer- or Parkinson-associated protein particles?
Review in Acta neuropathologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
- Cerebral amyloid angiopathy decades after red blood cell transfusions: a report of two cases from a prospective cohort.European journal of neurology · 2024Article
- Article
- Propagation of CJD Prions in Primary Murine Glia Cells Expressing Human PrPPathogens (Basel, Switzerland) · 2021Article
- Review
- Transmissible α-synuclein seeding activity in brain and stomach of patients with Parkinson's disease.Acta neuropathologica · 2021Article
- Aged Cattle Brain Displays Alzheimer's Disease-Like Pathology and Promotes Brain Amyloidosis in a Transgenic Animal Model.Frontiers in aging neuroscience · 2021Article
- Kinetics of α-synuclein prions preceding neuropathological inclusions in multiple system atrophy.PLoS pathogens · 2020Article
- From Synaptic Protein to Prion: The Long and Controversial Journey of α-Synuclein.Frontiers in synaptic neuroscience · 2020Review
- Alpha-synuclein: prion or prion-like?Acta neuropathologica · 2019Article
- Encephalopathy induced by Alzheimer brain inoculation in a non-human primate.Acta neuropathologica communications · 2019Article
- Molecular mechanisms of proteinopathies across neurodegenerative disease: a review.Neurological research and practice · 2019Review
- Prion-Like Mechanisms in Parkinson's Disease.Frontiers in neuroscience · 2019Review
- Mechanisms of protein toxicity in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2018Review
- Cellular mechanisms responsible for cell-to-cell spreading of prions.Cellular and molecular life sciences : CMLS · 2018Review
- Is multiple system atrophy an infectious disease?Annals of neurology · 2018Article
- Amyloidogenesis of Tau protein.Protein science : a publication of the Protein Society · 2017Review
- Spreading of Pathology in Alzheimer's Disease.Neurotoxicity research · 2017Review
- Implications of peptide assemblies in amyloid diseases.Chemical Society reviews · 2017Review
- Alpha-synuclein and iron: two keys unlocking Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2017Review
- Aβ seeds and prions: How close the fit?Prion · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The misfolding and aggregation of endogenous proteins in the central nervous system is a neuropathological hallmark of Alzheimer's disease (AD), Parkinson's disease (PD), as well as prion diseases. A molecular mechanism referred to as "nucleation-dependent aggregation" is thought to underlie this neuropathological phenomenon. According to this concept, disease-associated protein particles act as nuclei, or seeds, that recruit cellular proteins and incorporate them, in a misfolded form, into their growing aggregate structure. Experimental studies have shown that the aggregation of the AD-associated proteins amyloid-β (Aβ) and tau, and of the PD-associated protein α-synuclein, can be stimulated in laboratory animal models by intracerebral (i.c.) injection of inocula containing aggregated species of the respective proteins. This has raised the question of whether AD or PD can be transmitted, like certain human prion diseases, between individuals by self-propagating protein particles potentially present on medical instruments or in blood or blood products. While the i.c. injection of inocula containing AD- or PD-associated protein aggregates was found to cause neuronal damage and clinical abnormalities (e.g., motor impairments) in some animal models, none of the studies published so far provided evidence for a transmission of severe or even fatal disease. In addition, available epidemiological data do not indicate a transmissibility of AD or PD between humans. The findings published so far on the effects of experimentally transmitted AD- or PD-associated protein seeds do not suggest specific precautionary measures in the context of hemotherapy, but call for vigilance in transfusion medicine and other medical areas.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.