ArticleThe American journal of pathology2011
Neuroprotective effects of the cellular prion protein in autoimmune optic neuritis.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Co-modulation of TNFR1 and TNFR2 in an animal model of multiple sclerosis.Journal of neuroinflammation · 2023Article
- Prions and prion diseases: Insights from the eye.Experimental eye research · 2020Review
- Early auto-immune targeting of photoreceptor ribbon synapses in mouse models of multiple sclerosis.EMBO molecular medicine · 2018Article
- Anti-TNFR1 targeting in humanized mice ameliorates disease in a model of multiple sclerosis.Scientific reports · 2018Article
- Examining the Neural and Astroglial Protective Effects of Cellular Prion Protein Expression and Cell Death Protease Inhibition in Mouse Cerebrocortical Mixed Cultures.Molecular neurobiology · 2016Article
- Cellular prion protein promotes post-ischemic neuronal survival, angioneurogenesis and enhances neural progenitor cell homing via proteasome inhibition.Cell death & disease · 2015Article
- Neuroinflammation by cytotoxic T-lymphocytes impairs retrograde axonal transport in an oligodendrocyte mutant mouse.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the pathologic role of the prion protein in transmissible spongiform encephalopathic diseases has been widely investigated, the physiologic role of the cellular prion protein (PrP(C)) is not known. Among the many functions attributed to PrP(C), there is increasing evidence that it is involved in cell survival and mediates neuroprotection. A potential role in the immune response has also been suggested. However, how these two functions interplay in autoimmune disease is unclear. To address this, autoimmune optic neuritis, a model of multiple sclerosis, was induced in C57Bl/6 mice, and up-regulation of PrP(C) was observed throughout the disease course. In addition, compared with wild-type mice, in PrP(C)-deficient mice and mice overexpressing PrP(C), histopathologic analysis demonstrated that optic neuritis was exacerbated, as indicated by axonal degeneration, inflammatory infiltration, and demyelination. However, significant neuroprotection of retinal ganglion cells, the axons of which form the optic nerve, was observed in mice that overexpressed PrP(C). Conversely, mice lacking PrP(C) demonstrated significantly more neurodegeneration. This suggests that PrP(C) may have a neuroprotective function independent of its role in regulating the immune response.
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Registered trials
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.