Fabrizio Tagliavini

TL;DR: Solid phase immunoassay showed that a peptide homologous to residues 713 to 730 of beta PP770 bound tau proteins spontaneously formed fibrils in vitro and, in the presence of tau, generated dense fibrillary assemblies containing both molecules, suggesting that beta PP or beta PP fragments containing the tau binding site are involved in the pathogenesis of PHFs in Alzheimer's disease.

TL;DR: The pathogenetic mechanisms underlying tau mutations are reviewed, focusing on the less common aspects, so far poorly investigated, which suggest novel pathological features, such as a tendency to form oligomeric rather than fibrillar aggregates.

TL;DR: Plasma progranulin levels predict the presence of GRN null mutations independent of proximity to symptoms and brain atrophy, and correlations were found between age, years from average age at onset in each family, or TMEM106B rs1990622 genotype (p > 0.05).

TL;DR: A central and a virtual biobank for body fluids and associated data from subjects with neurodegenerative diseases have been established to support the validation of novel biomarkers and assays.

TL;DR: Early diagnosis allowing to treat at risk population in a preclinical stage represent the more realistic perspective for efficient TSE therapy.