Mitochondrial therapeutics in Alzheimer's disease and Parkinson's disease

被引：16

作者：

Hoekstra, Jake G. ^{[1
]}

Montine, Kathleen S. ^{[1
]}

Zhang, Jing ^{[1
]}

Montine, Thomas J. ^{[1
]}

机构：

[1] Univ Washington, Dept Pathol, Seattle, WA 98104 USA

来源：

ALZHEIMERS RESEARCH & THERAPY | 2011年 / 3卷 / 03期

基金：

美国国家卫生研究院;

关键词：

CYTOCHROME-C-OXIDASE; CELL-DEATH PATHWAYS; A-BETA; SYNAPTIC MITOCHONDRIA; SUBSTANTIA-NIGRA; MOUSE MODEL; BRAIN; DYSFUNCTION; PROTEIN; TOXICITY;

D O I：

10.1186/alzrt83

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

100204 [神经病学];

摘要：

In neurons, mitochondria serve a wide variety of processes that are integral to their function and survival. It is, therefore, not surprising that evidence of mitochondrial dysfunction is observed across numerous neurodegenerative diseases. Alzheimer's disease and Parkinson's disease are two such diseases in which aberrant mitochondrial activity is proposed to contribute to pathogenesis. Current therapies for each disease target various mechanisms, but few, if any, directly target improved mitochondrial function. Recent discoveries pertaining to mitochondrial dynamics reveal that regulation of mitochondrial fission and fusion may play a key role in the pathogenesis of these diseases and consequently could be novel future therapeutic targets.

引用

页数：7

共 64 条

[1]

Alam ZI, 1997, J NEUROCHEM, V69, P1326

[2]

Oxidative DNA damage in the parkinsonian brain: An apparent selective increase in 8-hydroxyguanine levels in substantia nigra [J].

Alam, ZI ;

Jenner, A ;

Daniel, SE ;

Lees, AJ ;

Cairns, N ;

Marsden, CD ;

Jenner, P ;

Halliwell, B .

JOURNAL OF NEUROCHEMISTRY, 1997, 69 (03) :1196-1203

[3]

Synaptic degeneration in Alzheimer's disease [J].

Arendt, Thomas .

ACTA NEUROPATHOLOGICA, 2009, 118 (01) :167-179

[4]

Neurodegenerative Pathways in Parkinson's Disease: Therapeutic Strategies [J].

Cardoso, S. M. ;

Moreira, P., I ;

Agostinho, P. ;

Pereira, C. ;

Oliveira, C. R. .

CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS, 2005, 4 (04) :405-419

[5]

Mitochondria dysfunction of Alzheimer's disease cybrids enhances Aβ toxicity [J].

Cardoso, SM ;

Santana, I ;

Swerdlow, RH ;

Oliveira, CR .

JOURNAL OF NEUROCHEMISTRY, 2004, 89 (06) :1417-1426

[6]

Alzheimer Disease [J].

Castellani, Rudy J. ;

Rolston, Raj K. ;

Smith, Mark A. .

DM DISEASE-A-MONTH, 2010, 56 (09) :484-546

[7]

Emerging functions of mammalian mitochondrial fusion and fission [J].

Chen, HC ;

Chan, DC .

HUMAN MOLECULAR GENETICS, 2005, 14 :R283-R289

[8]

Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin [J].

Clark, Ira E. ;

Dodson, Mark W. ;

Jiang, Changan ;

Cao, Joseph H. ;

Huh, Jun R. ;

Seol, Jae Hong ;

Yoo, Soon Ji ;

Hay, Bruce A. ;

Guo, Ming .

NATURE, 2006, 441 (7097) :1162-1166

[9]

Copper-dependent inhibition of human cytochrome c oxidase by a dimeric conformer of amyloid-β1-42 [J].

Crouch, PJ ;

Blake, R ;

Duce, JA ;

Ciccotosto, GD ;

Li, QX ;

Barnham, KJ ;

Curtain, CC ;

Cherny, RA ;

Cappai, R ;

Dyrks, T ;

Masters, CL ;

Trounce, IA .

JOURNAL OF NEUROSCIENCE, 2005, 25 (03) :672-679

[10]

Parkinson's disease: Mechanisms and models [J].

Dauer, W ;

Przedborski, S .

NEURON, 2003, 39 (06) :889-909

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