Finally, comparative biochemical studies of amyloid plaques isolated from human AD brains and APP transgenic mouse models have also shown that N-truncated Aβ peptides are much more prevalent in patients with AD, and it has been proposed that the greater abundance of N-truncated Aβ peptides is at least in part responsible for the substantially lower solubility of amyloid plaque material from humans [35, 36]. The gene discussed is APP; the disease is Alzheimer disease.