@misc{oai:repo.qst.go.jp:00070694,
 author = {前田, 純 and 樋口, 真人 and 須原, 哲也 and 前田 純 and 樋口 真人 and 須原 哲也},
 month = {Sep},
 note = {In vivo neuromolecular imaging technology has been markedly reinforced by application of positron emission tomography (PET) to genetically engineered animal models of neuropsychiatric disorders, by taking advantages of this imaging modality in quantitative reconstruction of signals and flexible designing of specific probes. On this basis, we provide the first evidence for the capability of a high-resolution PET imaging system in quantitatively mapping amyloid accumulation in living amyloid precursor protein transgenic (Tg) mice. It is also noteworthy that the localization and abundance of [11C]PIB autoradiographic signals were closely associated with those of N-terminally truncated and modified Abeta, AbetaN3-pyroglutamate, in Alzheimers disease (AD) and Tg mouse brains, implying that the detectability of amyloid by [11C]PIB positron emission tomography is dependent on the accumulation of specific Abeta subtypes. Our results support the usefulness of the small animal-dedicated PET system in conjunction with high-specific radioactivity probes and appropriate Tg models not only for clarifying the mechanistic properties of amyloidogenesis in mouse models., 生体機能と創薬シンポジウム 2008},
 title = {βアミロイド産生マウスを用いたβアミロイドリガンド[11C]PIBの結合機序の解明},
 year = {2008}
}