Impaired mitochondrial function in psychiatric disorders

被引：347

作者：

Manji, Husseini ^{[1
]}

Kato, Tadafumi ^{[2
]}

Di Prospero, Nicholas A. ^{[1
]}

Ness, Seth ^{[1
]}

Beal, M. Flint ^{[3
]}

Krams, Michael ^{[1
]}

Chen, Guang ^{[1
]}

机构：

[1] Janssen Res & Dev LLC, Raritan, NJ 08869 USA

[2] RIKEN Brain Sci Inst, Wako, Saitama 3510198, Japan

[3] Cornell Univ, Weill Med Coll, New York, NY 10021 USA

来源：

NATURE REVIEWS NEUROSCIENCE | 2012年 / 13卷 / 05期

关键词：

BIPOLAR AFFECTIVE-DISORDER; MAGNETIC-RESONANCE-SPECTROSCOPY; COMPLEX-I ACTIVITY; PROGRESSIVE EXTERNAL OPHTHALMOPLEGIA; EXTRACELLULAR-SUPEROXIDE DISMUTASE; DORSOLATERAL PREFRONTAL CORTEX; POSTMORTEM FRONTAL-CORTEX; MAJOR DEPRESSIVE DISORDER; GLUTATHIONE-S-TRANSFERASE; ELECTRON-TRANSPORT CHAIN;

D O I：

10.1038/nrn3229

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Major psychiatric illnesses such as mood disorders and schizophrenia are chronic, recurrent mental illnesses that affect the lives of millions of individuals. Although these disorders have traditionally been viewed as 'neurochemical diseases', it is now clear that they are associated with impairments of synaptic plasticity and cellular resilience. Although most patients with these disorders do not have classic mitochondrial disorders, there is a growing body of evidence to suggest that impaired mitochondrial function may affect key cellular processes, thereby altering synaptic functioning and contributing to the atrophic changes that underlie the deteriorating long-term course of these illnesses. Enhancing mitochondrial function could represent an important avenue for the development of novel therapeutics and also presents an opportunity for a potentially more efficient drug-development process.

引用

页码：293 / 307

页数：15

共 180 条

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