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Journal ArticleDOI

Evidence for a mitochondrial oxidative phosphorylation defect in brains from patients with schizophrenia

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TLDR
A defect of oxidative phosphorylation in brains from patients with schizophrenia is confirmed, which may contribute to impaired energy generation.
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This article is published in Schizophrenia Research.The article was published on 2001-03-01. It has received 198 citations till now. The article focuses on the topics: Temporal cortex & Respiratory chain.

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Molecular evidence for mitochondrial dysfunction in bipolar disorder.

TL;DR: Findings point toward a widespread dysregulation of mitochondrial energy metabolism and downstream deficits of adenosine triphosphate-dependent processes in bipolar disorder.
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Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis

TL;DR: Analysis of postmortem brains of patients with bipolar disorder or SZ found a global down-regulation of mitochondrial genes, such as those encoding respiratory chain components, in BD and SZ samples, even after the effect of sample pH was controlled, but this was likely due to the effects of medication.
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Gene Expression Profiling Reveals Alterations of Specific Metabolic Pathways in Schizophrenia

TL;DR: Molecular analyses implicate a highly specific pattern of metabolic alterations in the PFC of subjects with schizophrenia and raise the possibility that antipsychotic medications may exert a therapeutic effect, in part, by normalizing some of these changes.
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Mitochondrial complex I activity and oxidative damage to mitochondrial proteins in the prefrontal cortex of patients with bipolar disorder.

TL;DR: Impairment of complex I may be associated with increased protein oxidation and nitration in the prefrontal cortex of patients with bipolar disorder, and complex I activity and mitochondrial dysfunction may be potential therapeutic targets for bipolar disorder.
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Mitochondrial Dysfunction and Psychiatric Disorders

TL;DR: Energy impairment as a mechanism underlying the pathophysiology of some psychiatric disorders, like bipolar disorder, depression and schizophrenia, is discussed.
References
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Journal Article

Protein Measurement with the Folin Phenol Reagent

TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
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Sequence and organization of the human mitochondrial genome

TL;DR: The complete sequence of the 16,569-base pair human mitochondrial genome is presented and shows extreme economy in that the genes have none or only a few noncoding bases between them, and in many cases the termination codons are not coded in the DNA but are created post-transcriptionally by polyadenylation of the mRNAs.
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Aging, energy, and oxidative stress in neurodegenerative diseases.

TL;DR: Potential therapeutic approaches include glutamate release inhibitors, excitatory amino acid antagonists, strategies to improve mitochondrial function, free radical scavengers, and trophic factors, which appear promising in experimental studies and are now being applied to human studies.
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Mitochondrial genetics: a paradigm for aging and degenerative diseases?

TL;DR: Application of the hypothesis that a variety of degenerative processes may be associated with defects in oxidative phosphorylation has provided new insights into such diverse clinical problems as ischemic heart disease, late-onset diabetes, Parkinson's Disease, Alzheimer's disease, and aging.
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Decline in skeletal muscle mitochondrial respiratory chain function : possible factor in ageing

TL;DR: A substantial fall in mitochondrial oxidative capacity in ageing muscle is suggested, which may contribute to reduced exercise capacity in elderly people and contribute to the ageing process in other organs.
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