SEITA Yasunari
,
MORIMURA Toshifumi
,
WATANABE Naoki
,
IWATANI Chizuru
,
TSUCHIYA Hideaki
,
NAKAMURA Shinichiro
,
SUZUKI Toshiharu
,
YANAGISAWA Daijiro
,
TSUKIYAMA Tomoyuki
,
NAKAYA Masataka
,
OKAMURA Eiichi
,
MUTO Masanaga
,
EMA Masatsugu
,
NISHIMURA Masaki
,
TOOYAMA Ikuo
,
清田 弥寿成
,
守村 敏史
,
渡邊 直希
,
岩谷 千鶴
,
土屋 英明
,
中村 紳一郎
,
柳沢 大治郎
,
築山 智之
,
中家 雅隆
,
岡村 永一
,
武藤 真長
,
西村 正樹
,
遠山 育夫
… Although several groups have developed transgenic mouse models overexpressing the human amyloid-β precursor protein (APP) gene with AD mutations, with and without presenilin mutations, as well as APP gene knock-in mouse models, these animals display amyloid pathology but do not show neurofibrillary tangles or neuronal loss. … This presumably is due to differences between the etiology of the aged-related human disease and the mouse models. …
IR