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Validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis

Altered mitochondrial electron transport chain function has been implicated in the pathophysiology and etiology of schizophrenia. To date, our previously published study (i.e. first cohort) is still the only study to demonstrate that mitochondrial electron transport chain is not altered in white blo...

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Autores principales: Wu, Abbie, Da Silva, Tania, Jacobson, Maya, Tagore, Abanti, Lalang, Nittha, Kiang, Michael, Mizrahi, Romina, Andreazza, Ana C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722130/
https://www.ncbi.nlm.nih.gov/pubmed/31481687
http://dx.doi.org/10.1038/s41598-019-49180-3
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author Wu, Abbie
Da Silva, Tania
Jacobson, Maya
Tagore, Abanti
Lalang, Nittha
Kiang, Michael
Mizrahi, Romina
Andreazza, Ana C.
author_facet Wu, Abbie
Da Silva, Tania
Jacobson, Maya
Tagore, Abanti
Lalang, Nittha
Kiang, Michael
Mizrahi, Romina
Andreazza, Ana C.
author_sort Wu, Abbie
collection PubMed
description Altered mitochondrial electron transport chain function has been implicated in the pathophysiology and etiology of schizophrenia. To date, our previously published study (i.e. first cohort) is still the only study to demonstrate that mitochondrial electron transport chain is not altered in white blood cells from individuals at clinical high risk for psychosis. Here, we aimed to replicate our previous findings with an independent set of samples and validate the levels of mitochondrial complex I-V content in individuals at clinical high risk for psychosis. We demonstrated that the second cohort (i.e. validation cohort) expressed similar results as the first cohort. We combined the first cohort study with the second cohort and once more validated a lack of differential levels in mitochondrial complex I-V content between the two groups. In addition, we were able to validate a correlation between complex III content and prodromal negative symptom severity when the two cohorts studies were combined. Additionally, a correlation between complex V content and prodromal disorganization symptom severity was found when the two cohorts were combined. In conclusion, our results showed that dysfunction of the mitochondrial electron transport chain is not detected in peripheral blood mononuclear cells of individuals in the putative prodromal stage of schizophrenia.
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spelling pubmed-67221302019-09-17 Validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis Wu, Abbie Da Silva, Tania Jacobson, Maya Tagore, Abanti Lalang, Nittha Kiang, Michael Mizrahi, Romina Andreazza, Ana C. Sci Rep Article Altered mitochondrial electron transport chain function has been implicated in the pathophysiology and etiology of schizophrenia. To date, our previously published study (i.e. first cohort) is still the only study to demonstrate that mitochondrial electron transport chain is not altered in white blood cells from individuals at clinical high risk for psychosis. Here, we aimed to replicate our previous findings with an independent set of samples and validate the levels of mitochondrial complex I-V content in individuals at clinical high risk for psychosis. We demonstrated that the second cohort (i.e. validation cohort) expressed similar results as the first cohort. We combined the first cohort study with the second cohort and once more validated a lack of differential levels in mitochondrial complex I-V content between the two groups. In addition, we were able to validate a correlation between complex III content and prodromal negative symptom severity when the two cohorts studies were combined. Additionally, a correlation between complex V content and prodromal disorganization symptom severity was found when the two cohorts were combined. In conclusion, our results showed that dysfunction of the mitochondrial electron transport chain is not detected in peripheral blood mononuclear cells of individuals in the putative prodromal stage of schizophrenia. Nature Publishing Group UK 2019-09-03 /pmc/articles/PMC6722130/ /pubmed/31481687 http://dx.doi.org/10.1038/s41598-019-49180-3 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Wu, Abbie
Da Silva, Tania
Jacobson, Maya
Tagore, Abanti
Lalang, Nittha
Kiang, Michael
Mizrahi, Romina
Andreazza, Ana C.
Validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis
title Validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis
title_full Validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis
title_fullStr Validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis
title_full_unstemmed Validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis
title_short Validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis
title_sort validating mitochondrial electron transport chain content in individuals at clinical high risk for psychosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722130/
https://www.ncbi.nlm.nih.gov/pubmed/31481687
http://dx.doi.org/10.1038/s41598-019-49180-3
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