Ovariectomy and 17β-estradiol modulate disease progression of a mouse model of ALS

被引：54

作者：

Groeneveld, GJ

Van Muiswinkel, FL

Sturkenboomb, JM

Wokke, JHJ

Bär, PR

Van den Berg, LH

机构：

[1] Univ Utrecht, Med Ctr, Rudolf Magnus Inst Neurosci, Dept Neurol, NL-3508 GA Utrecht, Netherlands

[2] Univ Utrecht, Med Ctr, Rudolf Magnus Inst Neurosci, Lab Expt Neurol, Utrecht, Netherlands

来源：

BRAIN RESEARCH | 2004年 / 1021卷 / 01期

关键词：

E2; gonadal hormone; anti-oxidative; G93A; MND;

D O I：

10.1016/j.brainres.2004.06.024

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The incidence of amyotrophic lateral sclerosis (ALS) is higher among men than women but rises in women after the menopause. Estrogens may play a protective role. Treatment with estrogens has been shown to be neuroprotective in models of several neurodegenerative diseases. We therefore determined the effect of ovariectomy on female G93A mSOD1 transgenic mice, and the effect of subsequent treatment with 17beta-estradiol (E2). Ovariectomy led to a significant acceleration of disease progression of the mice, and high-dose E2 treatment significantly delayed disease progression of ovariectomized G93A mSOD1 transgenic mice. We conclude that treatment with E2 may also delay disease progression of post-menopausal women with ALS. (C) 2004 Elsevier B.V. All rights reserved.

引用

收藏

页码：128 / 131

页数：4

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