It was first described that neuroserpin was associated to Aβ plaques in the brain of AD patients, and in vitro work showed that neuroserpin formed a 1:1 binary complex with the N-terminal or middle part of the Aβ(1–42) peptide, leading to the inactivation of neuroserpin as an inhibitor of tPA, preventing the heat-induced polymerization of neuroserpin, altering Aβ oligomerisation to a non-fibrillary species, and rendering Aβ peptides less toxic to neuronal cells in culture [60]. The gene discussed is PLAT; the disease is Alzheimer disease.