A study of altered gene expression in frontal cortex from schizophrenic patients using differential screening

Mulcrone, Janet; Whatley, Stephen A.; Ferrier, I. N.; Marchbanks, R. M.

doi:10.1016/0920-9964(94)00040-f

Cited by 39 publications

(22 citation statements)

References 45 publications

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“…However, these two lines of study are not consistent with each other since activity of complex IV was unchanged 63 or decreased 64 in the frontal lobes, while mRNA expression of complex IV increased in the frontal lobes, 62 putamen, 67 and nucleus accumbens 67 and decreased in the caudate. 67 Furthermore, antipsychotics decreased COII expression, while increasing COX activity.…”

Section: Schizophreniamentioning

confidence: 68%

“…However, the sensitivity of cytochrome c oxidase to azide and the sensitivity of NADH-cytochrome c reductase to rotenone was decreased in brains of schizophrenic patients. 63 Cavelier and colleagues 64 at Uppsala University examined cytochrome oxidase activity in the brains of schizophrenic patients postmortem and compared them with those of patients with Alzheimer's disease. Activity was significantly decreased in caudate (63%) and frontal cortex (43%) in schizophrenic patients compared with controls.…”

Section: Schizophreniamentioning

confidence: 99%

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The other, forgotten genome: mitochondrial DNA and mental disorders

Kato

2001

Mol Psychiatry

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This paper summarizes recent research on mitochondrial DNA (mtDNA)-which might be described as the 'other, forgotten genome'. Recent studies suggest the possible pathophysiological significance of mtDNA in schizophrenia and neurodegenerative and mood disorders. Decreased activity of the mitochondrial electron transport chain has been implicated in both Parkinson's and Alzheimer's disease and while age-related accumulation of mtDNA deletions has been suggested as a possible cause, there is no concrete evidence that particular mtDNA polymorphisms are responsible. In schizophrenia, the activity and/or mRNA expression of complex IV are involved, but the direction of the alteration is not the same and there is no evidence linking schizophrenia with mtDNA. In bipolar disorder, there is some evidence of parent-of-origin effects and association with mtDNA polymorphisms but further investigation is needed to elucidate the role of mtDNA in mental disorders. Molecular Psychiatry (2001) 6, 625-633.

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Section: Schizophreniamentioning

confidence: 68%

Section: Schizophreniamentioning

confidence: 99%

The other, forgotten genome: mitochondrial DNA and mental disorders

Kato

2001

Mol Psychiatry

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“…Six studies have found altered mitochondriarelated gene expression in the prefrontal or frontal cortex in schizophrenia [Mulcrone et al, 1995;Whatley et al, 1996;Middleton et al, 2002;Karry et al, 2004;Prabakaran et al, 2004;Iwamoto et al, 2005;Shao et al, 2008]. Most found lower gene expression, including the two studies that adjusted for pH [Altar et al, 2005;Shao et al, 2008].…”

Section: Evidence For Mitochondrial Abnormalities and Dysfunction In mentioning

confidence: 94%

The mitochondrial genome and psychiatric illness

Anglin

Mazurek

Tarnopolsky

et al. 2012

American J of Med Genetics Pt B

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Psychiatric disorders are a leading cause of morbidity and mortality, yet their underlying pathophysiology remains unclear. Searches for a genetic cause of bipolar disorder, schizophrenia, and major depressive disorder have yielded inconclusive results. There is increasing interest in the possibility that defects in the mitochondrial genome may play an important role in psychiatric illness. We undertook a review of the literature investigating mitochondria and adult psychiatric disorders. MEDLINE, PsycINFO, and EMBASE were searched from their inception through September 2011, and the reference lists of identified articles were reviewed for additional studies. While multiple lines of evidence, including clinical, genetic, ultrastructural, and biochemical studies, support the involvement of mitochondria in the pathophysiology of psychiatric illness, many studies have methodological limitations and their findings have not been replicated. Clinical studies suggest that psychiatric features can be prominent, and the presenting features of mitochondrial disorders. There is limited but inconsistent evidence for the involvement of mitochondrial DNA haplogroups and mitochondria-related nuclear gene polymorphisms, and for mitochondrial ultrastructural and biochemical abnormalities in psychiatric illness. The current literature suggests that mitochondrial dysfunction and mitochondrial genetic variations may play an important role in psychiatric disorders, but additional methodologically rigorous and adequately powered studies are needed before definitive conclusions can be drawn.

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“…Subtractive cDNA libraries (Johnston-Wilson and Yolken, unpublished observations) 28 show an excess of mitochondrial messages in the brains of some individuals with schizophrenia. The role of these mitochondrial enzymes in the etiology of psychiatric disorders deserves additional consideration.…”

Section: Discussionmentioning

confidence: 99%

Disease-specific alterations in frontal cortex brain proteins in schizophrenia, bipolar disorder, and major depressive disorder

Cd²,

Jp³

et al. 2000

Mol Psychiatry

493

272

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Severe psychiatric disorders such as schizophrenia, bipolar disorder and major depressive disorder are brain diseases of unknown origin. No biological marker has been documented at the pathological, cellular, or molecular level, suggesting that a number of complex but subtle changes underlie these illnesses. We have used proteomic technology to survey postmortem tissue to identify changes linked to the various diseases. Proteomics uses two-dimensional gel electrophoresis and mass spectrometric sequencing of proteins to allow the comparison of subsets of expressed proteins among a large number of samples. This form of analysis was combined with a multivariate statistical model to study changes in protein levels in 89 frontal cortices obtained postmortem from individuals with schizophrenia, bipolar disorder, major depressive disorder, and non-psychiatric controls. We identified eight protein species that display disease-specific alterations in level in the frontal cortex. Six show decreases compared with the non-psychiatric controls for one or more diseases. Four of these are forms of glial fibrillary acidic protein (GFAP), one is dihydropyrimidinase-related protein 2, and the sixth is ubiquinone cytochrome c reductase core protein 1. Two spots, carbonic anhydrase 1 and fructose biphosphate aldolase C, show increase in one or more diseases compared to controls. Proteomic analysis may identify novel pathogenic mechanisms of human neuropsychiatric diseases. Molecular Psychiatry (2000) 5, 142-149.

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A study of altered gene expression in frontal cortex from schizophrenic patients using differential screening

Cited by 39 publications

References 45 publications

The other, forgotten genome: mitochondrial DNA and mental disorders

The other, forgotten genome: mitochondrial DNA and mental disorders

The mitochondrial genome and psychiatric illness

Disease-specific alterations in frontal cortex brain proteins in schizophrenia, bipolar disorder, and major depressive disorder

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