Androgen receptor and Kennedy disease/spinal bulbar muscular atrophy

被引：21

作者：

Monks, Douglas Ashley ^{[1
,2
]}

Rao, Pengcheng ^{[1
]}

Mo, Kaiguo ^{[1
]}

Johansen, Jamie Ann ^{[3
]}

Lewis, Gareth ^{[1
]}

Kemp, Michael Quentin ^{[3
]}

机构：

[1] Univ Toronto, Dept Psychol, Mississauga, ON L5L 1C6, Canada

[2] Univ Toronto, Inst Med Sci, Toronto, ON M5S 1A1, Canada

[3] Michigan State Univ, Neurosci Program, E Lansing, MI 48824 USA

来源：

HORMONES AND BEHAVIOR | 2008年 / 53卷 / 05期

关键词：

neuromuscular systems; sexual dimorphism; testosterone; axonopathy; myopathy; polyglutamine disease;

D O I：

10.1016/j.yhbeh.2007.12.009

中图分类号：

B84 [心理学]; C [社会科学总论]; Q98 [人类学];

学科分类号：

03 ; 0303 ; 030303 ; 04 ; 0402 ;

摘要：

Kennedy Disease/Spinal Bulbar Muscular Atrophy (KD/SBMA) is a progressive neurodegenerative disease caused by genetic polyglutamine expansion of the androgen receptor. We have recently found that overexpression of wildtype androgen receptor in skeletal muscle of transgenic mice results in a KD/SBMA phenotype. This surprising result challenges the orthodox view that KD/SBMA requires expression of polyglutamine expanded androgen receptor within motoneurons. Theories relating to the etiology of this disease drawn from studies of human patients, cellular and mouse models are considered with a special emphasis on potential myogenic contributions to as well as the molecular etiology of KD/SBMA. (c) 2008 Published by Elsevier Inc.

引用

页码：729 / 740

页数：12

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