It was first reported that neuroserpin binds to tPA in the brain of patients with Alzheimer’s disease, where it is associated with amyloid plaque formation; it is hypothesized that the amplified neuroserpin activity could result in a decrease in tPA function, which correlates with a diminished production of plasmin that may lead to a reduction in the dissolution of amyloid-beta aggregates in the brain tissue and a decline in synaptic activity and cognitive function [24,25]. This evidence concerns the gene PLAT and early-onset autosomal dominant Alzheimer disease.