Impaired neurotransmitter systems by Aβ amyloidosis in APPsw transgenic mice overexpressing amyloid β protein precursor

被引：28

作者：

Tomidokoro, Y ^{[1
]}

Harigaya, Y ^{[1
]}

Matsubara, E ^{[1
]}

Ikeda, M ^{[1
]}

Kawarabayashi, T ^{[1
]}

Okamoto, K ^{[1
]}

Shoji, M ^{[1
]}

机构：

[1] Gunma Univ, Sch Med, Dept Neurol, Maebashi, Gumma 371, Japan

来源：

NEUROSCIENCE LETTERS | 2000年 / 292卷 / 03期

关键词：

Alzheimer's disease; A beta; transgenic mice; somatostatin; substance P; choline acetyltransferase;

D O I：

10.1016/S0304-3940(00)01443-9

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

APPsw transgenic mice showing substantial features of brain A beta amyloidosis such as senile plaques and behavioral abnormalities were examined by immunostaining to determine whether A beta deposits could induce the subsequent disturbance of neurotransmitter systems including somatostatin, substance P and choline acety]transferase (ChAT), which are prominent in the Alzheimer's disease brain. Somatostatin, substance P and ChAT disappeared in the areas of senile plaque and were accumulated in dystrophic neurites around the amyloid cores. These findings suggest a potential role of brain A beta amyloidosis in disturbance of the neurotransmitter systems leading to memory disturbance of Alzheimer's disease. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：155 / 158

页数：4

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