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Although prion infections cause cognitive impairment and neuronal death, transcriptional and translational profiling shows progressive derangement within glia but surprisingly little changes within neurons. Here we expressed PrP
selectively in neurons and astrocytes of mice. After prion infection, both astrocyte and neuron-restricted PrP
expression led to copious brain accumulation of PrP
. As expected, neuron-restricted expression was associated with typical prion disease. However, mice with astrocyte-restricted PrP
expression experienced a normal life span, did not develop clinical disease, and did not show astro- or microgliosis. Besides confirming that PrP
is innocuous to PrP
-deficient neurons, these results show that astrocyte-born PrP
does not activate the extreme neuroinflammation that accompanies the onset of prion disease and precedes any molecular changes of neurons. This points to a nonautonomous mechanism by which prion-infected neurons instruct astrocytes and microglia to acquire a specific cellular state that, in turn, drives neural dysfunction.
Sprache
Englisch
Identifikatoren
ISSN: 1015-6305
eISSN: 1750-3639
DOI: 10.1111/bpa.13056
Titel-ID: cdi_crossref_primary_10_1111_bpa_13056
Format
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