@misc{oai:repo.qst.go.jp:00070053,
 author = {季, 斌 and 前田, 純 and 澤田, 誠 and 小野, 麻衣子 and 岡内, 隆 and 張, 明栄 and 鈴木, 和年 and Ｔｒｏｊａｎｏｗｓｋｉ, Ｊｏｈｎ Ｑ． and Ｌｅｅ, Ｖｉｒｇｉｎｉａ Ｍ．−Ｙ． and 樋口, 真人 and 須原, 哲也 and 季 斌 and 前田 純 and 澤田 誠 and 小野 麻衣子 and 岡内 隆 and 張 明栄 and 鈴木 和年 and 樋口 真人 and 須原 哲也},
 month = {May},
 note = {Recent advances in neuroimaging technology have permitted in-vivo visualization of peripheral benzodiazepine receptor (PBR) upregulated in a subset of activated microglia and astrocytes, while links between PBR expression and pathophysiological effects of gliosis are yet to be elucidated. In order to clarify the glial responses underlying PBR-positivity, we investigated the cellular expression of PBR in diverse animal models of neuropathologies, including transgenics recapitulating two pathological hallmarks of Alzheimer's disease (AD), senile plaques and fibrillary tau lesions, by means of autoradiographic and immunohistochemical methods. In mice overexpressing mutant amyloid precursor protein (APP), amyloid b deposition was concurrent with astrocyte-dominant PBR expression. This was in remarkable contrast to PBR upregulation in non-astroglial components responding to accumulation of phosphorylated tau in mutant tau transgenic mice. In consideration of unremarkable neuronal depopulation in APP transgenics and massive neuronal loss in tau transgenics, we postulated that differential localization of PBR in these models reflected deleterious and beneficial glial reactions to tau versus Abeta pathologies, respectively. As a support of this presumption, analyses of experimental models of non-AD neuropathologies, including excitotoxicity, demyelination and nigrostriatal dopaminergic injuries, revealed that reversible neuronal damages are characterized by PBR-positive astrocytosis coupled with PBR-negative microgliosis, and that irreversible neurotoxicity is accompanied by PBR-negative astrocytosis uncoupled with overt microgliosis or coexistent with PBR-positive microgliosis. Mechanistic involvement of nontoxic microgliosis in astrocytic PBR expression was also demonstrated by intracranial transplantation of immortalized microglial cells. Furthermore, beneficial roles of PBR-positive astrocytes were indicated by general coincidence of PBR and glial cell line-derived neurotrophic factor upregulations in the animal models examined here. These findings support the utility of PBR as a biomarker for pathogenic and therapeutic implications of gliosis in AD and other neurodegenerative conditions., 第4回日本分子イメージング学会学術集会},
 title = {※},
 year = {2009}
}