Emergence of immunoreactivities for phosphorylated tau and amyloid-β protein in chronic stage of fluid percussion injury in rat brain

被引：51

作者：

Hoshino, S

Tamaoka, A

Takahashi, M

Kobayashi, S

Furukawa, T

Oaki, Y

Mori, O

Matsuno, S

Shoji, S

Inomata, M

Teramoto, A

机构：

[1] Chiba Hokusoh Hosp, Nippon Med Sch, Dept Neurosurg, Chiba 27016, Japan

[2] Chiba Hokusoh Hosp, Nippon Med Sch, Dept Pathol, Chiba 27016, Japan

[3] Univ Tsukuba, Inst Clin Med, Dept Neurol, Tsukuba, Ibaraki 305, Japan

[4] Yamanouchi Pharmaceut Co Ltd, Tokyo, Japan

[5] Nippon Med Sch, Hlth Sci Res Inst, Tokyo, Japan

[6] Nippon Med Sch, Dept Neurosurg, Tokyo, Japan

来源：

NEUROREPORT | 1998年 / 9卷 / 08期

关键词：

Alzheimer's disease; amyloid-beta protein; brain injury; rat; tau;

D O I：

10.1097/00001756-199806010-00039

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

HEAD injury is one of the potential environmental factors in Alzheimer's disease (AD). To study the chronic stage of concussive brain injury, histological analyses were performed 2-6 months after right lateral fluid percussion (FP) brain injury (3.6-4.8 atm) in rats. Six months after injury, numerous normal-looking neurons in the telencephalon and brain stem were immunoreactive with either antibody to phosphorylated tau or with four antibodies to beta-amyloid protein. Neuronal counts in the cortices were gradually decreased after injury, up to 42% loss at 6 months after injury. These neuropathological changes suggest that this animal model could serve as a good animal model of neurodegenerative diseases such as AD. (C) 1998 Rapid Science Ltd.

引用

页码：1879 / 1883

页数：5

共 25 条

[21] BETA-AMYLOID PROTEIN DEPOSITION IN THE BRAIN AFTER SEVERE HEAD-INJURY - IMPLICATIONS FOR THE PATHOGENESIS OF ALZHEIMERS-DISEASE [J].