The difference in serum proteomes in schizophrenia and bipolar disorder

Smirnova, L.; Seregin, A.; Boksha, Irina S.; Dmitrieva, E. Yu.; Симуткин, Г. Г.; Kornetova, E.; Savushkina, Olga K.; Letova, Anastasia; Бохан, Н. А.; Ivanova, Svetlana A.; Zgoda, Victor G.

doi:10.1186/s12864-019-5848-1

Cited by 32 publications

(65 citation statements)

References 95 publications

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“…Gray matter decreases in the anterior cingulate have been reported as markers of genetic liability to psychosis, while reductions in the superior temporal gyrus and cerebellum may be the first onset of the disease markers [22]. Quantitative proteomic analysis using mass spectrometry identified 27 proteins specific to schizophrenia [23].…”

Section: Discussionmentioning

confidence: 99%

Amino Acid and Acylcarnitine Levels in Chronic Patients with Schizophrenia: A Preliminary Study

et al. 2021

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Amino acids and acylcarnitines play an important role as substrates and intermediate products in most of pathways involved in schizophrenia development such as mitochondrial dysfunction, inflammation, lipid oxidation, DNA damage, oxidative stress, and apoptosis. It seems relevant to use an integrated approach with ‘omics’ technology to study their contribution. The aim of our study was to investigate serum amino acid and acylcarnitine levels in antipsychotics-treated patients with chronic schizophrenia compared with healthy donors. We measured serum levels of 15 amino acids and 30 acylcarnitines in 37 patients with schizophrenia and 36 healthy donors by means of tandem mass spectrometry. In summary, patients with chronic schizophrenia had an altered concentration of a few amino acids and acylcarnitines in comparison to the healthy probands. Further research is needed to assess and understand the identified changes.

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Section: Discussionmentioning

confidence: 99%

Amino Acid and Acylcarnitine Levels in Chronic Patients with Schizophrenia: A Preliminary Study

et al. 2021

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“…A recent study from our group identified differentially expressed proteins in the serum of individuals with amphetamine use disorder compared with a healthy control group [ 23 ]. Moreover, prior clinical proteomic studies utilized serum samples to determine the levels of proteins in patients who had developed neurodegenerative diseases [ 24 , 25 ], neurodevelopmental disorders [ 26 , 27 , 28 ], major depressive disorder, and bipolar disorders [ 29 , 30 ]. In the present study, we investigate the expression changes of CUD patients’ serum proteins compared with healthy controls, using an untargeted proteomic approach employing two-dimensional (2D) alteration in gel electrophoresis (2D-DIGE) coupled with mass spectroscopy (MS).…”

Section: Introductionmentioning

confidence: 99%

Serum Proteomic Analysis of Cannabis Use Disorder in Male Patients

et al. 2021

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Cannabis use has been growing recently and it is legally consumed in many countries. Cannabis has a variety of phytochemicals including cannabinoids, which might impair the peripheral systems responses affecting inflammatory and immunological pathways. However, the exact signaling pathways that induce these effects need further understanding. The objective of this study is to investigate the serum proteomic profiling in patients diagnosed with cannabis use disorder (CUD) as compared with healthy control subjects. The novelty of our study is to highlight the differentially changes proteins in the serum of CUD patients. Certain proteins can be targeted in the future to attenuate the toxicological effects of cannabis. Blood samples were collected from 20 male individuals: 10 healthy controls and 10 CUD patients. An untargeted proteomic technique employing two-dimensional difference in gel electrophoresis coupled with mass spectrometry was employed in this study to assess the differentially expressed proteins. The proteomic analysis identified a total of 121 proteins that showed significant changes in protein expression between CUD patients (experimental group) and healthy individuals (control group). For instance, the serum expression of inactive tyrosine protein kinase PEAK1 and tumor necrosis factor alpha-induced protein 3 were increased in CUD group. In contrast, the serum expression of transthyretin and serotransferrin were reduced in CUD group. Among these proteins, 55 proteins were significantly upregulated and 66 proteins significantly downregulated in CUD patients as compared with healthy control group. Ingenuity pathway analysis (IPA) found that these differentially expressed proteins are linked to p38MAPK, interleukin 12 complex, nuclear factor-κB, and other signaling pathways. Our work indicates that the differentially expressed serum proteins between CUD and control groups are correlated to liver X receptor/retinoid X receptor (RXR), farnesoid X receptor/RXR activation, and acute phase response signaling.

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“…It is noteworthy that the top pathways for diurnal rhythms in prefrontal cortex gene expression that were different in schizophrenia compared to healthy controls are oxidative phosphorylation and mitochondrial dysfunction [ 99 ]. The results of proteomic studies also confirm gene expression dysregulation in schizophrenia [ 100 – 102 ]. Prabakaran et al showed that almost half of the proteins with altered expression were associated with oxidative stress responses and mitochondrial function [ 103 ].…”

Section: Molecular Mechanisms Of Oxidative Stress In the Pathogenementioning

confidence: 63%

Oxidative Stress‐Related Mechanisms in Schizophrenia Pathogenesis and New Treatment Perspectives

Ermakov

Dmitrieva

Parshukova

et al. 2021

Oxidative Medicine and Cellular Longevity

123

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Schizophrenia is recognized to be a highly heterogeneous disease at various levels, from genetics to clinical manifestations and treatment sensitivity. This heterogeneity is also reflected in the variety of oxidative stress-related mechanisms contributing to the phenotypic realization and manifestation of schizophrenia. At the molecular level, these mechanisms are supposed to include genetic causes that increase the susceptibility of individuals to oxidative stress and lead to gene expression dysregulation caused by abnormal regulation of redox-sensitive transcriptional factors, noncoding RNAs, and epigenetic mechanisms favored by environmental insults. These changes form the basis of the prooxidant state and lead to altered redox signaling related to glutathione deficiency and impaired expression and function of redox-sensitive transcriptional factors (Nrf2, NF-κB, FoxO, etc.). At the cellular level, these changes lead to mitochondrial dysfunction and metabolic abnormalities that contribute to aberrant neuronal development, abnormal myelination, neurotransmitter anomalies, and dysfunction of parvalbumin-positive interneurons. Immune dysfunction also contributes to redox imbalance. At the whole-organism level, all these mechanisms ultimately contribute to the manifestation and development of schizophrenia. In this review, we consider oxidative stress-related mechanisms and new treatment perspectives associated with the correction of redox imbalance in schizophrenia. We suggest that not only antioxidants but also redox-regulated transcription factor-targeting drugs (including Nrf2 and FoxO activators or NF-κB inhibitors) have great promise in schizophrenia. But it is necessary to develop the stratification criteria of schizophrenia patients based on oxidative stress-related markers for the administration of redox-correcting treatment.

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The difference in serum proteomes in schizophrenia and bipolar disorder

Cited by 32 publications

References 95 publications

Amino Acid and Acylcarnitine Levels in Chronic Patients with Schizophrenia: A Preliminary Study

Amino Acid and Acylcarnitine Levels in Chronic Patients with Schizophrenia: A Preliminary Study

Serum Proteomic Analysis of Cannabis Use Disorder in Male Patients

Oxidative Stress‐Related Mechanisms in Schizophrenia Pathogenesis and New Treatment Perspectives

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