Mitotic and gender parallels in Alzheimer disease: Therapeutic opportunities

被引:5
|
作者
Zhu, X
Webber, KM
Casadesus, G
Raina, AK
Lee, HG
Marlatt, M
Hartzler, A
Atwood, CS
Bowen, R
Perry, G
Smith, MA
机构
[1] Case Western Reserve Univ, Inst Pathol, Cleveland, OH 44106 USA
[2] Univ Wisconsin, Madison, WI USA
[3] William S Middleton Mem Vet Adm, Madison, WI USA
[4] Voyager Pharmaceut Corp, Raleigh, NC USA
关键词
Alzheimer disease; amyloid-beta; cell cycle; leuprolide acetate; luteinizing hormone; oxidative stress; tau phosphorylation;
D O I
10.2174/1389450043345317
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
In this review, we discuss the role of cell cycle dysfunction in the pathogenesis of Alzheimer disease and propose that such mitotic catastrophe, as one of the earliest events in neuronal degeneration. may, in fact. be sufficient to initiate the neurodegenerative cascade. The question as to what molecule initiates cell cycle dysfunction is now beginning to become understood and, in this regard, the gender-predication, age-related penetrance and regional Susceptibility of specific neuronal populations led us to consider luteinizing hormone as a key mediator of the abnormal mitotic process. As such, agents targeted toward luteinizing hormone or downstream sequelae may be of great therapeutic value in the treatment of Alzheimer disease.
引用
收藏
页码:559 / 563
页数:5
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