Plasma Soluble P-selectin, Interleukin-6 and S100B Protein in Patients with Schizophrenia: a Pilot Study

Pinjari, Omar F.; Dasgupta, Swapan; Okusaga, Olaoluwa

doi:10.1007/s11126-021-09954-3

Cited by 6 publications

(11 citation statements)

References 48 publications

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“…Importantly, activated platelets are capable of affecting the structural integrity of the BBB [29], penetrate and interact with the cellular components of the BBB matrix including astrocytes [30]. Relatedly, we found a positive correlation between plasma sP-selectin, and the astrocyte marker, S100B in patients with schizophrenia [17]. Moreover, schizophrenia is now considered a neurodevelopmental and neurodegenerative disorder [7] and astrocytes have been shown to contribute to progression of neurodegeneration in neurodegenerative disorders [31].…”

Section: Discussion/conclusionmentioning

confidence: 86%

“…Using previously collected data on a sample of 106 non-veteran patients [17] with schizophrenia enrolled in a non-metabolic syndrome study (at the time of discharge from inpatient psychiatric treatment), we identified patients that met criteria for MetS (MetS+). The criteria used for MetS were the combination of overweight/obesity, plasma TG > 150 mg/dL, and HDL < 40 mg/dL).…”

Section: Methodsmentioning

confidence: 99%

“…Assessment of platelet activation by flow cytometry [16] and plasma sP-selectin [17] respectively, have been reported in schizophrenia but to our knowledge, the association of platelet activation with MetS and cognition in schizophrenia has not been reported. We therefore evaluated platelet activation, and cognitive assessments in two independent pilot samples of patients with schizophrenia or schizoaffective disorder with differing MetS status.…”

Section: Introductionmentioning

confidence: 99%

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Is platelet activation a link between metabolic syndrome and cognitive impairment in patients with schizophrenia?

Okusaga

Vijayan

Rumbaut

2023

Preprint

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Introduction: Schizophrenia is a severe psychiatric condition associated with cognitive impairment and premature dementia. Furthermore, metabolic syndrome (MetS)-combined central obesity, diabetes, dyslipidemia and hypertension-is highly prevalent in patients with schizophrenia and is believed to contribute to cognitive impairment and premature dementia in patients with schizophrenia. However, the mechanisms by which MetS contributes to cognitive impairment in patients with schizophrenia is unclear. Based on the association of MetS with platelet activation and the ability of activated platelets to impact blood-brain-barrier function, we tested the hypothesis that platelet activation is associated with both MetS and cognitive impairment in two independent pilot samples of patients with schizophrenia. Methods: In the first pilot sample (sample A) we recruited 13 veterans with either schizophrenia or schizoaffective disorder with MetS (MetS+, n=6), and without MetS (MetS-, n=7). We administered the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB) on all 13 veterans and assessed platelet activation using flow cytometry. In the second pilot sample (sample B), we identified 10 non-veteran MetS+ patients with schizophrenia and 10 age-, and sex-matched MetS- patients with schizophrenia from previously collected data on 106 patients enrolled in a non-MetS study. Participants in sample B had data on the NIH Toolbox cognitive battery (NIH Toolbox) and plasma soluble P-selectin (sP-selectin), a marker of platelet activation. We compared flow cytometry platelet activation in MetS+ and MetS- using the Mann Whitney test and the median test to compare sP-selectin and cognitive measures. We also measured the correlation between platelet activation and cognition using Spearman's rho correlation. Results: Platelet activation was significantly higher in MetS+ than MetS- (mean rank 8.60 vs. 3.83, p=0.017). Median score for the picture vocabulary test (language ability) was significantly lower in MetS+ relative to MetS- (82.35 vs. 104, p=0.015). In addition, platelet activation correlated negatively (rho = -0.74, p= 0.009) with the Wechsler Memory Scale: Spatial Span (nonverbal working memory) and plasma sP-selectin correlated negatively (rho = -0.55, p= 0.029) with the List Sorting Working Memory Test. Conclusion: Our preliminary findings suggest that platelet activation is involved in the association of MetS with cognitive impairment in patients with schizophrenia. Future studies are needed to elucidate the role of platelets in MetS-related cognitive impairment in patients with schizophrenia.

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Section: Discussion/conclusionmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Is platelet activation a link between metabolic syndrome and cognitive impairment in patients with schizophrenia?

Okusaga

Vijayan

Rumbaut

2023

Preprint

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“…A total of 28 articles were used to write the systematic review. Of these articles, 20 focused on astrocyte analysis ( Hagenauer et al, 2018 ; O’Donovan et al, 2018 ; López-González et al, 2019 ; Amoah et al, 2020 ; Chan et al, 2020 ; Karpiński et al, 2020 ; Kindler et al, 2020 ; Rodrigues-Amorim et al, 2020 ; Zhang et al, 2020 ; Corley et al, 2021 ; Jeon et al, 2021 ; Ranganathan et al, 2021 ; Shimamoto-Mitsuyama et al, 2021 ; Uranova et al, 2021 ; Di Biase et al, 2022 ; Endres et al, 2022 ; Huang et al, 2022 ; Pinjari et al, 2022 ; Schmitt et al, 2022 ; Zong et al, 2023 ), and 18 focused on microglia analysis ( Hagenauer et al, 2018 ; López-González et al, 2019 ; Adorjan et al, 2020 ; Karpiński et al, 2020 ; Kindler et al, 2020 ; Petrasch-Parwez et al, 2020 ; Uranova et al, 2020 , 2021 ; Zhang et al, 2020 ; Corley et al, 2021 ; Hill et al, 2021 ; Jiang et al, 2021 ; Shimamoto-Mitsuyama et al, 2021 ; Di Biase et al, 2022 ; Vikhreva and Uranova, 2022 ; Jenkins et al, 2023 ; Yu et al, 2023 ; Zong et al, 2023 ). Importantly, on the total of the researches concerning astroglia and microglia measures, 10 evaluated both aspects.…”

Section: Resultsmentioning

confidence: 99%

The role of glial cells in mental illness: a systematic review on astroglia and microglia as potential players in schizophrenia and its cognitive and emotional aspects

Laricchiuta,

Papi,

Decandia

et al. 2024

Front. Cell. Neurosci.

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Schizophrenia is a complex and severe mental disorder that affects approximately 1% of the global population. It is characterized by a wide range of symptoms, including delusions, hallucinations, disorganized speech and behavior, and cognitive impairment. Recent research has suggested that the immune system dysregulation may play a significant role in the pathogenesis of schizophrenia, and glial cells, such as astroglia and microglia known to be involved in neuroinflammation and immune regulation, have emerged as potential players in this process. The aim of this systematic review is to summarize the glial hallmarks of schizophrenia, choosing as cellular candidate the astroglia and microglia, and focusing also on disease-associated psychological (cognitive and emotional) changes. We conducted a systematic review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We searched PubMed, Scopus, and Web of Science for articles that investigated the differences in astroglia and microglia in patients with schizophrenia, published in the last 5 years. The present systematic review indicates that changes in the density, morphology, and functioning of astroglia and microglia may be involved in the development of schizophrenia. The glial alterations may contribute to the pathogenesis of schizophrenia by dysregulating neurotransmission and immune responses, worsening cognitive capabilities. The complex interplay of astroglial and microglial activation, genetic/epigenetic variations, and cognitive assessments underscores the intricate relationship between biological mechanisms, symptomatology, and cognitive functioning in schizophrenia.

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“…21 Researchers tracking TSPO changes in relation to BBB alteration have not seen elevated binding in schizophrenia, change due to stage of disease course, or differentiation from low-grade inflammation. [21][22][23][24] Moreover, TSPO may be confounded by antipsychotic use 25 and microglial expression did not correlate with any changes in adhesion molecules. 13 TSPO is not an ideal indicator of microglial activation due to BBB breakdown, but that does not bar the possibility of at least a partial contribution to the development of schizophrenia.…”

Section: The Role Of Microglia In Bbb Dysfunctionmentioning

confidence: 87%

Faulty fences: Blood-brain barrier dysfunction in schizophrenia

Schrenk¹

2022

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he blood-brain barrier (BBB) is an essential barrier of closely spaced cells that regulates entry into the CNS. What passes should be highly regulated to protect the brain from potentially harmful peripheral cells or molecules from the rest of the body. However, research has revealed that the BBB is pathologically permeable in several disease states, including schizophrenia, epilepsy, traumatic brain injury, autism, and DiGeorge syndrome (22q11.2 deletion syndrome, which often presents with symptoms of schizophrenia). 1,2 In this article, we discuss potential markers of BBB dysfunction, the consequences of a porous BBB, the effect of BBB permeability on microglial activation, and possible treatment implications.

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Plasma Soluble P-selectin, Interleukin-6 and S100B Protein in Patients with Schizophrenia: a Pilot Study

Cited by 6 publications

References 48 publications

Is platelet activation a link between metabolic syndrome and cognitive impairment in patients with schizophrenia?

Is platelet activation a link between metabolic syndrome and cognitive impairment in patients with schizophrenia?

The role of glial cells in mental illness: a systematic review on astroglia and microglia as potential players in schizophrenia and its cognitive and emotional aspects

Faulty fences: Blood-brain barrier dysfunction in schizophrenia

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