Abnormal Mitochondrial Dynamics-A Novel Therapeutic Target for Alzheimer's Disease?

被引：61

作者：

Su, Bo ^{[1
]}

Wang, Xinglong ^{[1
]}

Bonda, David ^{[1
]}

Perry, Gorge ^{[1
,2
]}

Smith, Mark ^{[1
]}

Zhu, Xiongwei ^{[1
]}

机构：

[1] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA

[2] Univ Texas San Antonio, Coll Sci, San Antonio, TX 78249 USA

来源：

MOLECULAR NEUROBIOLOGY | 2010年 / 41卷 / 2-3期

关键词：

Alzheimer's disease; Mitochondrial dynamics; Mitochondrial fission; Mitochondrial fusion; Drug; Dimebon; DEPENDENT PROTEIN-KINASE; CASPASE-CLEAVED TAU; ALPHA-LIPOIC ACID; CALCIUM HOMEOSTASIS; AMYLOID-BETA; ENDOPLASMIC-RETICULUM; MISSENSE MUTATIONS; FUSION MEDIATORS; OXIDATIVE DAMAGE; ALTERED CALCIUM;

D O I：

10.1007/s12035-009-8095-7

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Mitochondria are dynamic organelles that undergo continuous fission and fusion, which could affect all aspects of mitochondrial function. Mitochondrial dysfunction has been well documented in Alzheimer's disease (AD). In the past few years, emerging evidence indicates that an imbalance of mitochondrial dynamics is involved in the pathogenesis of AD. In this review, we discuss in detail the abnormal mitochondrial dynamics in AD and how such abnormal dynamics may impact mitochondrial and neuronal function and contribute to the course of disease. Based on this discussion, we propose that mitochondrial dynamics could be a potential therapeutic target for AD.

引用

页码：87 / 96

页数：10

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