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Role of PrPC in neuronal differentiation and propagation of its infectious isoform PrPSc by microvesicles

Author: Maria Grazia Barenco Montrasio
Dissertation: Frankfurt (Main), University, Diss., 2008.
Edition/Format:   Computer file : Thesis/dissertation : English
Summary:
Prion diseases or transmissible spongiform encephalopathies (TSEs) are rare neurological disorders that may be of genetic or infectious origin, but most frequently occur sporadically in humans. Their outcome is invariably fatal. The infectious agent has been defined as prion (from proteinaceous infectious only) in 1992 by Stanley B. Prusiner and represent mainly, if not solely, an abnormal, protease-resistant  Read more...
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Details

Material Type: Thesis/dissertation, Internet resource
Document Type: Internet Resource, Computer File
All Authors / Contributors: Maria Grazia Barenco Montrasio
OCLC Number: 277049147
Description: Online-Ressource
Responsibility: von Maria Grazia Barenco Montrasio.

Abstract:

Prion diseases or transmissible spongiform encephalopathies (TSEs) are rare neurological disorders that may be of genetic or infectious origin, but most frequently occur sporadically in humans. Their outcome is invariably fatal. The infectious agent has been defined as prion (from proteinaceous infectious only) in 1992 by Stanley B. Prusiner and represent mainly, if not solely, an abnormal, protease-resistant isoform (PrPSc) of a cellular protein, the prion protein or PrPC. According to the protein onlyʺ hypothesis, the prion is devoid of informational nucleic acids and consists of an "infectious" protein that is capable of converting the normal host protein PrPC into a likeness of itself. TSEs can be distinguished from other neurodegenerative diseases because of their infectivity and transmission capability. The only organ system in which severe histopathological damage can be demonstrated as a consequence of infection with prions is the nervous system. The communal lesions are neuronal loss, spongiosis and astrogliosis, accompanied by an intra- and extracellular accumulation of PrPSc, occasionally in form of amyloid plaques. Even if a strong activation of microglia and astrocytes occurs, no immunological response is usually detectable as consequence of prion infection. ...

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