Abstract：
:Prion diseases are rare transmissible neurodegenerative disorders caused by the accumulation of a misfolded isoform (PrPSc) of the cellular prion protein (PrPC) in the central nervous system (CNS). Neuropathological hallmarks of prion diseases are neuronal loss, astrogliosis, and enhanced microglial proliferation and activation. As immune cells of the CNS, microglia participate both in the maintenance of the normal brain physiology and in driving the neuroinflammatory response to acute or chronic (e.g., neurodegenerative disorders) insults. Microglia involvement in prion diseases, however, is far from being clearly understood. During this review, we summarize and discuss controversial findings, both in patient and animal models, suggesting a neuroprotective role of microglia in prion disease pathogenesis and progression, or-conversely-a microglia-mediated exacerbation of neurotoxicity in later stages of disease. We also will consider the active participation of PrPC in microglial functions, by discussing previous reports, but also by presenting unpublished results that support a role for PrPC in cytokine secretion by activated primary microglia.
journal_name
Int J Mol Scijournal_title
International journal of molecular sciencesauthors
Peggion C,Stella R,Lorenzon P,Spisni E,Bertoli A,Massimino MLdoi
10.3390/ijms21207765subject
Has Abstractpub_date
2020-10-20 00:00:00issue
20issn
1422-0067pii
ijms21207765journal_volume
21pub_type
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journal_title：International journal of molecular sciences
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journal_title：International journal of molecular sciences
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journal_title：International journal of molecular sciences
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更新日期：2020-01-10 00:00:00
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journal_title：International journal of molecular sciences
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