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
Type: conference-paper
Abstract: 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 Alzheimer's 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 Abetasubtypes. 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.
Language: Japanese
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W7145642742