The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Mitochondrial dysfunction in schizophrenia: a possible linkage to dopamine
Open accessAbstract
Mitochondria are not only the principal source of high energy intermediates, but play an important role in intracellular calcium buffering, are main producers of reactive oxygen species, and are the source of pro‐ and antiapoptotic key factors. Moreover, the mitochondria are of a ubiquitous nature and the respiratory chain has a dual genetic basis, i.e. the mitochondrial and the nuclear DNAs. Thus mitochondrial impairment could provide an explanation for the tremendous heterogeneity of clinical and pathological manifestations in schizophrenia. This article reviews several independent lines of evidence that suggest an involvement of mitochondrial dysfunction in schizophrenia. Among them are altered cerebral energy metabolism, mitochondrial hypoplasia, dysfunction of the oxidative phosphorylation system and altered mitochondrial related gene expression. In addition, the interaction between dopamine, a predominant etiological factor in schizophrenia, and mitochondrial respiration is considered as a possible mechanism underlying the hyper‐ and hypo‐activity cycling in schizophrenia. Understanding the role of mitochondria in schizophrenia may encourage novel treatment approaches, the identification of candidate genes and new insights into the pathophysiology and etiology of the disorder.
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Citations
Cites
A review of MRI findings in schizophrenia
Shenton, M. E., Dickey, C. C., Frumin, M., & McCarley, R. W. (2001) · Schizophrenia Research · doi:10.1016/s0920-9964(01)00163-3 · Cited by 2,346
Mitochondrial Complex I Deficiency in Parkinson's Disease
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Dopamine Receptor Binding Predicts Clinical and Pharmacological Potencies of Antischizophrenic Drugs
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“Hyperactivity of the dopaminergic neurons has been shown by imaging studies to be associated with increased synthesis and release of dopamine (Breier et al. 1997; Laruelle et al. 1999; Lindstrom et al. 1999).”
BackgroundSeeman, P., & Lee, T. (1975) · Science · doi:10.1126/science.1145194 · Cited by 869
Cytochrome oxidase deficiency in Alzheimer’s disease
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Neurotransmitter interactions in schizophrenia–therapeutic implications
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Cited by
Schizophrenia genes, gene expression, and neuropathology: on the matter of their convergence
Harrison, P. J., & Weinberger, D. R. (2005) · Molecular Psychiatry · doi:10.1038/sj.mp.4001558 · Cited by 2,020
Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism
Golomb, B. A., & Evans, M. A. (2008) · American Journal of Cardiovascular Drugs · doi:10.2165/0129784-200808060-00004 · Cited by 677
Mitochondrial dysfunction and pathology in bipolar disorder and schizophrenia
Clay, H. B., Daws, S., & Konradi, C. (2011) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2010.08.007 · Cited by 399
Mitochondrial alterations of retinal pigment epithelium in age-related macular degeneration
Feher, J., Kovacs, I., Artico, M., Cavallotti, C., Papale, A., & Balacco Gabrieli, C. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.05.012 · Cited by 388
Altar, C. A., Jurata, L. W., Charles, V., Lemire, A., Liu, P., Bukhman, Y., Young, T. A., Bullard, J., Yokoe, H., Webster, M. J., et al. (2005) · Biological Psychiatry · doi:10.1016/j.biopsych.2005.03.031 · Cited by 318
Metadata
- Authors
- Ben‐Shachar, D.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2002-12
- Volume
- 83
- Issue
- 6
- Pages
- 1241-1251
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1585966888
- Cited by
- 222
- References
- 7
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
