@article{oai:repo.qst.go.jp:00047313,
 author = {Bing, Wang and Tanaka, Kaoru and Ji, Bin and Ono, Maiko and Hou, Yagun and Ninomiya, Yasuharu and Maruyama, Kouichi and Izumi-Nakajima, Nakako and Begum, Nasrin and Higuchi, Makoto and Fujimori, Akira and Uehara, Yoshihiko and Nakajima, Tetsuo and Suhara, Tetsuya and Nenoi, Mitsuru and 王 冰 and 田中 薫 and 季 斌 and 小野 麻衣子 and 方 雅群 and 二宮 康晴 and 丸山 耕一 and 中島 菜花子 and ＢＥＧＵＭ ＮＡＳＲＩＮ and 樋口 真人 and 藤森 亮 and 中島 徹夫 and 須原 哲也 and 根井 充},
 issue = {7},
 journal = {Journal of Neuroscience Research},
 month = {May},
 note = {The cause and risk factors of Alzheimer’s disease (AD) are largely unknown. Studies on possible radiation-induced AD-like pathogenesis and behavioral consequences are important as humans are exposed to ionizing radiation (IR) from various sources. It was reported that total body irradiations (TBI) at 10 cGy of low linear energy transfer (LET) X-rays to mice triggered acute transcriptional alterations in genes associated with cognitive dysfunctions. However, it was unknown if low doses of IR could induce AD-like changes late after exposure. We reported previously that 10 cGy X-rays induced early transcriptional response of several AD-related genes in hippocampi without late AD-like pathogenesis and memory impairment in mice. Here further studies on two low doses (5 cGy or 10 cGy) of high LET carbon-ion irradiations are reported. On expression of 84 AD-related genes in hippocampi, at 4 hours after TBI, 5 cGy induced a significant up-regulation of 3 genes (Abca1, Casp3 and Chat), 10 cGy lead to a marked up-regulation of 1 gene (Chat) and a down-regulation of 3 genes (Apoe, Ctsd and Il1a), while at 1 year after TBI, 1 gene (Il1a) was significantly down-regulated in 10 cGy-irradiated animals. Changes in spatial learning ability and memory, and induction of AD-like pathogenesis were not detected by in vivo brain imaging for amyloid beta peptide accumulation and by immunohistochemical staining of amyloid precursor protein, amyloid beta protein, tau and phosphorylated tau protein. These findings indicate that low doses of carbon-ion irradiations did not cause behavioral impairment and AD-like pathological change in mice.},
 pages = {915--926},
 title = {Low-dose total body carbon-ion irradiations induce early transcriptional alteration without late Alzheimer's disease-like pathogenesis and memory impairment in mice.},
 volume = {92},
 year = {2014}
}