While the complex of GM1 and Aβ, termed GAβ, identified in AD brains seems to act as an endogenous seed for the Aβ fibrillogenesis in the AD brain [44,45,46,47,48], administration of intraventricular GM1 resulted in a reduction in Aβ level in the brain and marked improvements in several clinical outcomes, which suggests that GM1 might serve as a therapeutic agent [49]. The gene discussed is A1BG; the disease is Alzheimer disease.