Geraldina Riccardi

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In order to assess the susceptibility of bank voles to chronic wasting disease (CWD), we inoculated voles carrying isoleucine or methionine at codon 109 (Bv109I and Bv109M, respectively) with CWD isolates from elk, mule deer and white-tailed deer. Efficient transmission rate (100%) was observed with mean survival times ranging from 156 to 281 days post(More)
Gerstmann-Sträussler-Scheinker disease (GSS) is an inherited neurodegenerative disorder associated with mutations in the prion protein gene and accumulation of misfolded PrP with protease-resistant fragments (PrP(res)) of 6-8 kDa. With the exception of a few GSS cases characterized by co-accumulation of PrP(res) of 21 kDa, efforts to transmit GSS to rodents(More)
It is widely known that prion strains can mutate in response to modification of the replication environment and we have recently reported that prion mutations can occur in vitro during amplification of vole-adapted prions by Protein Misfolding Cyclic Amplification on bank vole substrate (bvPMCA). Here we exploited the high efficiency of prion replication by(More)
Previously, Multimer Detection System (MDS) detected scrapie infected lambs of 8 mo age at pre-clinical stage in comparison with the normal controls. Above lamb were born from scrapie infected parent sheep (VRQ/VRQ). Here, MDS was challenged twice blindly with scrapie sheep blood samples from pre-clinical stages. These sheep showed no symptoms and they died(More)
The ability of PrP to convert PrP into protease-resistance isoforms has been exploited using a variety of techniques such as protein misfolding cyclic amplification (PMCA), quaking induced conversion (QuIC) and most recently, real-time quaking induced conversion (RT-QuIC). These cell-free assays have enabled a better understanding of prion diseases and have(More)
Prion diseases are rare neurodegenerative conditions associated with the conformational conversion of the cellular prion protein (PrP(C)) into PrP(Sc), a self-replicating isoform (prion) that accumulates in the central nervous system of affected individuals. The structure of PrP(Sc) is poorly defined, and likely to be heterogeneous, as suggested by the(More)
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