Morbidity Risk of Schizophrenia to Parents and Siblings of Schizophrenic Patients

Shimizu, Akinori; Kurachi, Masayoshi; Yamaguchi, Nariyoshi; Torii, Hosaku; Isaki, Kiminori

doi:10.1111/j.1440-1819.1987.tb00392.x

Cited by 27 publications

(23 citation statements)

References 9 publications

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“…Species-specific sperm mitochondria are believed to be eliminated via ubiquination, which tags them for breakdown through proteolysis (15). Interestingly, there is some evidence for high maternal transmission of SZ (16)(17)(18)(19), as well as BPD (20), which supports the hypothesis that increased risk for these disorders is related to mitochondrial dysfunction. However, it is also possible that this relationship may be due to environmental factors (21).…”

Section: Introductionsupporting

confidence: 64%

Mitochondrial involvement in psychiatric disorders

et al. 2008

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Recent findings of mitochondrial abnormalities in brains from subjects with neurological disorders have led to a renewed search for mitochondrial abnormalities in psychiatric disorders. A growing body of evidence suggests that there is mitochondrial dysfunction in schizophrenia, bipolar disorder, and major depressive disorder, including evidence from electron microscopy, imaging, gene expression, genotyping, and sequencing studies. Specific evidence of dysfunction such as increased common deletion and decreased gene expression in mitochondria in psychiatric illnesses suggests that direct examination of mitochondrial DNA from postmortem brain cells may provide further details of mitochondrial alterations in psychiatric disorders.

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Section: Introductionsupporting

confidence: 64%

Mitochondrial involvement in psychiatric disorders

et al. 2008

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“…Although there has been no convincing evidence for an exclusively maternal transmission of SCZ, several reports suggest a higher maternal transmission of SCZ [79-82]. …”

Section: Resultsmentioning

confidence: 99%

Paradox of schizophrenia genetics: is a paradigm shift occurring?

Doi

Hoshi

Itokawa

et al. 2012

Behavioral and Brain Functions

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BackgroundGenetic research of schizophrenia (SCZ) based on the nuclear genome model (NGM) has been one of the most active areas in psychiatry for the past two decades. Although this effort is ongoing, the current situation of the molecular genetics of SCZ seems disappointing or rather perplexing. Furthermore, a prominent discrepancy between persistence of the disease at a relatively high prevalence and a low reproductive fitness of patients creates a paradox. Heterozygote advantage works to sustain the frequency of a putative susceptibility gene in the mitochondrial genome model (MGM) but not in the NGM.MethodsWe deduced a criterion that every nuclear susceptibility gene for SCZ should fulfill for the persistence of the disease under general assumptions of the multifactorial threshold model. SCZ-associated variants listed in the top 45 in the SZGene Database (the version of the 23rd December, 2011) were selected, and the distribution of the genes that could meet or do not meet the criterion was surveyed.Results19 SCZ-associated variants that do not meet the criterion are located outside the regions where the SCZ-associated variants that could meet the criterion are located. Since a SCZ-associated variant that does not meet the criterion cannot be a susceptibility gene, but instead must be a protective gene, it should be linked to a susceptibility gene in the NGM, which is contrary to these results. On the other hand, every protective gene on any chromosome can be associated with SCZ in the MGM. Based on the MGM we propose a new hypothesis that assumes brain-specific antioxidant defenses in which trans-synaptic activations of dopamine- and N-methyl-d-aspartate-receptors are involved. Most of the ten predictions of this hypothesis seem to accord with the major epidemiological facts and the results of association studies to date.ConclusionThe central paradox of SCZ genetics and the results of association studies to date argue against the NGM, and in its place the MGM is emerging as a viable option to account for genomic and pathophysiological research findings involving SCZ.

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“…43 Mode of inheritance There is some evidence to suggest higher maternal transmission of schizophrenia. [44][45][46] The reason for this is unclear and may reflect mitochondrial inheritance or differences in opportunity between the sexes for finding partners. 47 Comorbidity with mitochondrial disease Patients with MELAS sometimes demonstrate delusions and hallucinations due to delirium [48][49][50][51] or schizophrenialike symptoms.…”

Section: Schizophreniamentioning

confidence: 99%

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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Morbidity Risk of Schizophrenia to Parents and Siblings of Schizophrenic Patients

Cited by 27 publications

References 9 publications

Mitochondrial involvement in psychiatric disorders

Mitochondrial involvement in psychiatric disorders

Paradox of schizophrenia genetics: is a paradigm shift occurring?

The other, forgotten genome: mitochondrial DNA and mental disorders

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