Showing papers by "Fabrizio Tagliavini published in 1997"
TL;DR: In IDX-treated hamsters, clinical signs of disease were delayed and survival time was prolonged, and Neuropathological examination showed a parallel delay in the appearance of brain changes and in the accumulation of PrPres and PrP amyloid.
Abstract: Prion diseases are transmissible neurodegenerative conditions characterized by the accumulation of protease-resistant forms of the prion protein (PrP), termed PrPres, in the brain. Insoluble PrPres tends to aggregate into amyloid fibrils. The anthracycline 4'-iodo-4'-deoxy-doxorubicin (IDX) binds to amyloid fibrils and induces amyloid resorption in patients with systemic amyloidosis. To test IDX in an experimental model of prion disease, Syrian hamsters were inoculated intracerebrally either with scrapie-infected brain homogenate or with infected homogenate coincubated with IDX. In IDX-treated hamsters, clinical signs of disease were delayed and survival time was prolonged. Neuropathological examination showed a parallel delay in the appearance of brain changes and in the accumulation of PrPres and PrP amyloid.
180 citations
TL;DR: The ability of PrP 106-126 to increase membrane microviscosity was unrelated to the propensity of the peptide to raise fibrils, and speculated that the glial and nerve cell involvement occurring in prion-related encephalopathies might be caused by the interaction with the plasma membrane of a PrP106-126-like fragment or of the sequence spanning residues 106- 126 of the abnormal isoform of the prion protein.
61 citations
TL;DR: Findings point to the disorganization of most thalamic circuits as a condition necessary for the sleep-wake rhythm being affected.
31 citations