Cecília Monteiro

TL;DR: Persuasive pharmacological and genetic evidence now supports protein aggregation as the cause of postmitotic tissue dysfunction or loss, and a more detailed understanding of the factors that trigger and sustain aggregate formation is needed to develop future disease-modifying therapies.

TL;DR: Concomitant cardiac evaluation identified patients with involvement of the myocardium, allowing for implementation of disease-modifying therapy in patients undergoing carpal tunnel release surgery.

TL;DR: Novel strategies are required and the possibility of utilizing the chaperone BRICHOS to prevent Aβ aggregation and toxicity is discussed, and the drug tafamidis is available as a promising treatment.

TL;DR: Subunit exchange was used to quantify the stabilization of WT TTR from senile systemic amyloidosis patients currently being treated with tafamidis (20 mg orally, once daily), and TTR kinetic stability correlated with the tAFamidis plasma concentration.

TL;DR: The authors used peptide-based probes to identify misfolded transthyretin (TTR) oligomers in the plasma of TTR hereditary amyloidosis patients exhibiting a predominant neuropathic phenotype.