Roberto Chiesa

TL;DR: It is reported here that neuronal death results from chronic exposure of primary rat hippocampal cultures to micromolar concentrations of a peptide corresponding to residues 106–126 of the amino-acid sequence deduced from human PrP complementary DNA.

TL;DR: It is reported that, in mice, acute intracerebroventricular injections of synthetic Aβ1–42 oligomers impaired consolidation of the long-term recognition memory, whereas mature Aβ 1–42 fibrils and freshly dissolved peptide did not, and it was confirmed that A β1– 42 oligomers interact with PrPC, with nanomolar affinity.

TL;DR: The results confirm the potential pathogenic role of A beta in AD, and indicate that amyloid fibrils may induce neuronal death through a specific programmed process.

TL;DR: Transgenic mice that express the mouse homolog of a mutant human PrP containing a nine octapeptide insertion associated with prion dementia are produced, establishing a new transgenic animal model of an inherited human prion disorder.

TL;DR: It is reported here that mutant PrP molecules are delayed in their maturation to an endoglycosidase H-resistant form after biosynthetic labeling, suggesting that they are impaired in their exit from the endoplasmic reticulum (ER), but it is found that proteasome inhibitors have no effect on the maturation or turnover of either mutant or wild-type PrP molecule.