The Role of OXT, OXTR, AVP, and AVPR1a Gene Expression in the Course of Schizophrenia

Schizophrenia is a serious and chronic mental illness, the symptoms of which usually appear for the first time in late adolescence or early adulthood. To date, much research has been conducted on the etiology of schizophrenia; however, it is still not fully understood. Oxytocin and vasopressin as neuromodulators that regulate social and emotional behavior are promising candidates for determining the vulnerability to schizophrenia. The aim of this study was to evaluate the expression of OXT, OXTR, AVP, and AVPR1a genes at the mRNA and protein levels in patients with schizophrenia. Due to the neurodegenerative nature of schizophrenia, the study group was divided into two subgroups, namely, G1 with a diagnosis that was made between 10 and 15 years after the onset of the illness, and G2 with a diagnosis made up to two years after the onset of the illness. Moreover, the relationship between the examined genes and the severity of schizophrenia symptoms, assessed using PANSS (Positive and Negative Syndrome Scale) and CDSS scales (Clinical Depression Scale for Schizophrenia) was evaluated. The analysis of the expression of the studied genes at the mRNA and protein levels showed statistically significant differences in the expression of all the investigated genes. OXT and AVPR1a gene expression at both the mRNA and protein levels were significantly lower in the schizophrenia group, and OXTR and AVP gene expression at both the mRNA and protein levels was higher in the schizophrenia subjects than in the controls. Furthermore, a significant correlation of OXT gene expression at the mRNA and protein levels with the severity of depressive symptoms in schizophrenia as assessed by CDSS was found.

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Codon usage and protein sequence pattern dependency in different organisms: A Bioinformatics approach

Journal of Bioinformatics and Computational Biology ◽

10.1142/s021972001550002x ◽

2015 ◽

Vol 13 (02) ◽

pp. 1550002

Author(s):

Mohammad-Hadi Foroughmand-Araabi ◽

Bahram Goliaei ◽

Kasra Alishahi ◽

Mehdi Sadeghi ◽

Sama Goliaei

Keyword(s):

Gene Regulation ◽

Codon Usage ◽

Protein Sequence ◽

Multinomial Logistic Regression ◽

Translation Efficiency ◽

Translation Rate ◽

Protein Levels ◽

Synonymous Codons ◽

First Time

Although it is known that synonymous codons are not chosen randomly, the role of the codon usage in gene regulation is not clearly understood, yet. Researchers have investigated the relation between the codon usage and various properties, such as gene regulation, translation rate, translation efficiency, mRNA stability, splicing, and protein domains. Recently, a universal codon usage based mechanism for gene regulation is proposed. We studied the role of protein sequence patterns on the codons usage by related genes. Considering a subsequence of a protein that matches to a pattern or motif, we showed that, parts of the genes, which are translated to this subsequence, use specific ratios of synonymous codons. Also, we built a multinomial logistic regression statistical model for codon usage, which considers the effect of patterns on codon usage. This model justifies the observed codon usage preference better than the classic organism dependent codon usage. Our results showed that the codon usage plays a role in controlling protein levels, for genes that participate in a specific biological function. This is the first time that this phenomenon is reported.

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Abstract 285: Osteopontin Deficiency Ameliorates Heart Failure with Preserved Ejection Fraction Pathology by Upregulating Mitochondrial 2-Oxoglutarate Dehydrogenase Like Enzyme

Circulation Research ◽

10.1161/res.121.suppl_1.285 ◽

2017 ◽

Vol 121 (suppl_1) ◽

Author(s):

Keyvan Yousefi ◽

Wen Ding ◽

Lina A Shehadeh

Keyword(s):

Mouse Model ◽

Diastolic Dysfunction ◽

Interstitial Fibrosis ◽

Matricellular Protein ◽

Double Knockout ◽

Protein Levels ◽

Lower Protein ◽

Myocardial Energetics ◽

First Time

HFpEF is an increasingly prevalent syndrome associated with impaired myocardial energetics, for which no etiologic therapy is available. Osteopontin (OPN) is a matricellular protein that is upregulated in the circulation of HFpEF patients, and reported to induce mitochondrial stress in rodent cardiomyocytes. Here we evaluate the role of circulating OPN in regulating myocardial function in the nephrotic Col4a3 -/- mouse model of HFpEF. We performed extensive cardiac, biochemical and mitochondrial analyses of the Col4a3 -/- mouse and found a striking HFpEF phenotype. We showed OPN levels were elevated in Col4a3 -/- mice (FC=2.1, n=6; p<.01). Col4a3 -/- mice were hypertensive, had diastolic dysfunction, myocyte hypertrophy and interstitial fibrosis - all of which were ameliorated in Col4a3 -/- OPN -/- mice (n=5-20; p<.05). Col4a3 -/- hearts had dysmorphic mitochondria (EM), lowered antioxidant capacity as a 50% reduction in GSH/GSSG ratio (n=6; p<.05) and lower protein levels of mitochondrial respiratory complexes I, II and IV (p<.05). Flux assay in adult cardiomyocytes showed that maximal respiration was reduced in Col4a3 -/- hearts (575.84±37.6 vs 322.34±25.48 pmol/min in WT, n=9; p<.0001). Microarray data (validated by mitochondrial blot) implicated OGDHL as decreased in Col4a3 -/- hearts but increased in double knockout Col4a3 -/- OPN -/- hearts compared to WT (n=3; p<.05). OGDH activity was also lower in Col4a3 -/- hearts (17.1±7.3 vs 2.5±1.1 mU/mg in WT; n=6; p<.05). In Col4a3 -/- mice, heart-specific AAV9-mediated overexpression of OGDHL, similar to global OPN KO, improved survival by ~50-100% (p<.0001). Isovolumetric relaxation time, a marker of diastolic dysfunction, which is prolonged in Col4a3 -/- mice (26.17 vs 15.30±1 ms, n=26; p<.001) was decreased in Col4a3 -/- OPN -/- mice (18.1±1 ms, n=37; p<.01) as well as in AAV9-cTnT-OGDHL-treated Col4a3 -/- mice (16.7±2.5 ms, n=8; p<.05). In conclusion, we present a new mouse model for HFpEF in which diastolic function and lifespan can be improved by genetic deletion of OPN or cardiac OGDHL gene therapy. Our results elucidate for the first time the pivotal roles of circulating OPN and cardiac OGDHL in HFpEF pathophysiology and present two related potential therapeutic targets for HFpEF.

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Polyamines regulate gene expression by stimulating translation of histone acetyltransferase mRNAs

Journal of Biological Chemistry ◽

10.1074/jbc.ra120.013833 ◽

2020 ◽

Vol 295 (26) ◽

pp. 8736-8745 ◽

Cited By ~ 1

Author(s):

Akihiko Sakamoto ◽

Yusuke Terui ◽

Takeshi Uemura ◽

Kazuei Igarashi ◽

Keiko Kashiwagi

Keyword(s):

Gene Expression ◽

Regulation Of Gene Expression ◽

Histone Acetyltransferases ◽

Regulate Gene Expression ◽

Double Stranded Rna ◽

Protein Levels ◽

Lysine Residues ◽

Regulate Gene ◽

Stimulation Of

Polyamines regulate gene expression in Escherichia coli by translationally stimulating mRNAs encoding global transcription factors. In this study, we focused on histone acetylation, one of the mechanisms of epigenetic regulation of gene expression, to attempt to clarify the role of polyamines in the regulation of gene expression in eukaryotes. We found that activities of histone acetyltransferases in both the nucleus and cytoplasm decreased significantly in polyamine-reduced mouse mammary carcinoma FM3A cells. Although protein levels of histones H3 and H4 did not change in control and polyamine-reduced cells, acetylation of histones H3 and H4 was greatly decreased in the polyamine-reduced cells. Next, we used control and polyamine-reduced cells to identify histone acetyltransferases whose synthesis is stimulated by polyamines. We found that polyamines stimulate the translation of histone acetyltransferases GCN5 and HAT1. Accordingly, GCN5- and HAT1-catalyzed acetylation of specific lysine residues on histones H3 and H4 was stimulated by polyamines. Consistent with these findings, transcription of genes required for cell proliferation was enhanced by polyamines. These results indicate that polyamines regulate gene expression by enhancing the expression of the histone acetyltransferases GCN5 and HAT1 at the level of translation. Mechanistically, polyamines enhanced the interaction of microRNA-7648-5p (miR-7648-5p) with the 5′-UTR of GCN5 mRNA, resulting in stimulation of translation due to the destabilization of the double-stranded RNA (dsRNA) between the 5′-UTR and the ORF of GCN5 mRNA. Because HAT1 mRNA has a short 5′-UTR, polyamines may enhance initiation complex formation directly on this mRNA.

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Role of traditional healers in the pathway to care of patients with schizophrenia in Egypt

International Journal of Social Psychiatry ◽

10.1177/0020764020910456 ◽

2020 ◽

Vol 66 (4) ◽

pp. 382-388 ◽

Cited By ~ 3

Author(s):

Mona Ibrahim Awaad ◽

Nesreen Mohsen Ibrahim ◽

Rehab Mohamed Naguib ◽

Sherien Ahmed Khalil ◽

Mahmoud Elhabiby ◽

...

Keyword(s):

Help Seeking ◽

Traditional Healers ◽

Clinical Correlates ◽

Syndrome Scale ◽

Seeking Behavior ◽

Axis I ◽

Dsm Iv ◽

Negative Syndrome ◽

Pathway To Care

Background: Traditional healers are considered one of the important stages in the pathway to care of schizophrenia patients because of the confidence in the system, affordability and accessibility of the service, exposing patients to hazardous management, delay in seeking psychiatric help and bad prognosis. Aim: To assess the pathway to care of schizophrenia patients and role of traditional healers into it, the sociodemographic and clinical correlates of those patients. Methods: We assessed 232 patients with schizophrenia after confirmation of diagnosis with Structured Clinical Interview for DSM-IV Axis I Disorder (SCID-I) research version using a questionnaire designed by authors to assess help seeking behavior in schizophrenia patients and its sociodemographic and clinical correlates. Positive and Negative Syndrome Scale to identify the presence and severity of symptoms. Results: A total of 41.8% sought traditional healers first, 58.1% sought a psychiatric consultation first, main symptoms related to traditional healers seeking were hallucinations in 51.5%, delusions 29.9%, 9.28% bizarre behavior and 9.28% formal though disorder. Main causes of traditional healers’ preference were society acceptance 30.39%, affordability 24.74% and accessibility 16.49%. Conclusion: This study shows that a significant percentage of the patients suffering from schizophrenia prefer to approach faith healers first due to their own beliefs, society acceptance, affordability and easy accessibility.

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microRNA-422a Inhibits DCC Expression in a Manner Dependent on SNP rs12607853

Cytogenetic and Genome Research ◽

10.1159/000506031 ◽

2020 ◽

Vol 160 (2) ◽

pp. 63-71

Author(s):

Yunxiao Li ◽

Xugang Shi ◽

Xintong Cai ◽

Yongsheng Zhu ◽

Yuanyuan Chen ◽

...

Keyword(s):

Gene Expression ◽

Opioid Addiction ◽

Heroin Addiction ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Protein Levels ◽

Gene Assay ◽

New Biomarkers ◽

And Function

DCC netrin 1 receptor (DCC) affects the structure and function of the dopamine circuitry, which in turn affects the susceptibility to developing addiction. In a previous study, we found that single nucleotide polymorphism (SNP) rs12607853 in the 3′ untranslated region (3′-UTR) of DCC was significantly associated with heroin addiction. In the current study, we first used bioinformatics prediction to identify the DCC rs12607853 C allele as a potential hsa-miR-422a and hsa-miR-378c target site. We then used vector construction and dual-luciferase reporter assays to investigate the targeting relationship of DCC rs12607853 with hsa-miR-422a and hsa-miR-378c. The dual-luciferase reporter gene assay confirmed that the C allele of rs12607853 in combination with hsa-miR-422a led to repressed dual-luciferase gene expression. Moreover, gene expression assays disclosed that hsa-miR-422a inhibited DCC expression at both the mRNA and protein levels. We also found that morphine inhibited the expression of hsa-miR-422a but increased the expression of DCC mRNA, and this change in the expression of hsa-miR-422a could not be reversed by naloxone, which suggested that the role of DCC in opioid addiction might be regulated by hsa-miR-422a. In summary, this study improves our understanding of the role of hsa-miR-422a and identifies the genetic basis of rs12607853, which might contribute to the discovery of new biomarkers or therapeutic targets for opioid addiction.

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Hepatocyte Nuclear Factor 4 alpha (HNF4α) Activation is Essential for Termination of Liver Regeneration

10.1101/304808 ◽

2018 ◽

Author(s):

Ian Huck ◽

Sumedha Gunewardena ◽

Regina Espanol-Suner ◽

Holger Willenbring ◽

Udayan Apte

Keyword(s):

Gene Expression ◽

Liver Regeneration ◽

Target Gene ◽

Nuclear Factor ◽

Hepatocyte Nuclear Factor ◽

Hepatic Differentiation ◽

Target Gene Expression ◽

Protein Levels ◽

Hepatocyte Nuclear Factor 4

AbstractHepatocyte Nuclear Factor 4 alpha (HNF4α) is critical for hepatic differentiation. Recent studies have highlighted its role in inhibition of hepatocyte proliferation and tumor suppression. However, the role of HNF4α in liver regeneration is not known. We hypothesized that hepatocytes modulate HNF4α activity when navigating between differentiated and proliferative states during liver regeneration. Western blot analysis revealed a rapid decline in nuclear and cytoplasmic HNF4α protein levels accompanied with decreased target gene expression within 1 hour after 2/3 partial hepatectomy (post-PH) in C57BL/6J mice. HNF4α protein expression did not recover to the pre-PH levels until day 3. Hepatocyte-specific deletion of HNF4α (HNF4α-KO) in mice resulted in 100% mortality post-PH despite increased proliferative marker expression throughout regeneration. Sustained loss of HNF4α target gene expression throughout regeneration indicated HNF4α-KO mice were unable to compensate for loss of HNF4α transcriptional activity. Deletion of HNF4α resulted in sustained proliferation accompanied by c-myc and cyclin D1 over expression and a complete deficiency of hepatocyte function after PH. Interestingly, overexpression of degradation-resistant HNF4α in hepatocytes did not prevent initiation of regeneration after PH. Finally, AAV8-mediated reexpression of HNF4α in hepatocytes of HNF4α-KO mice post-PH restored HNF4α protein levels, induced target gene expression and improved survival of HNF4α-KO mice post-PH. In conclusion, these data indicate that HNF4α reexpression following initial decrease is critical for hepatocytes to exit from cell cycle and resume function during the termination phase of liver regeneration. These results reveal the role of HNF4α in liver regeneration and have implications for therapy of liver failure.

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Maternal postnatal depression and offspring depression at age 24 years in a UK-birth cohort: the mediating role of maternal nurturing behaviours concerning feeding, crying and sleeping

Wellcome Open Research ◽

10.12688/wellcomeopenres.17006.1 ◽

2021 ◽

Vol 6 ◽

pp. 187

Author(s):

Iryna Culpin ◽

Gemma Hammerton ◽

Marc H. Bornstein ◽

Jon Heron ◽

Jonathan Evans ◽

...

Keyword(s):

Birth Cohort ◽

Indirect Effect ◽

Postnatal Depression ◽

Early Adulthood ◽

Depression Scale ◽

Adverse Outcomes ◽

Birth Cohort Study ◽

Adult Offspring ◽

Probit Regression

Background: Maternal postnatal depression (PND) is a risk factor for offspring depression in adulthood. However, few longitudinal studies have examined the role of maternal nurturing parenting behaviours in the association between maternal PND and offspring depression in adulthood. Methods: We examined pathways from maternal PND measured using self-reported Edinburgh Postnatal Depression Scale at 8 weeks to offspring ICD-10 depression diagnosed using the Clinical Interview Schedule-Revised computerised assessment at 24 years through maternal-reported nurturing behaviours concerning feeding, sleeping and crying measured from pregnancy to age 3 years 6 months in 5,881 members of the UK-based birth cohort study, the Avon Longitudinal Study of Parents and Children. Results: The fully adjusted model revealed an indirect effect from PND to adult offspring depression through the combination of all parenting factors (probit regression coefficient [B]=0.038, 95% confidence interval [CI] 0.005, 0.071); however, there was no evidence of a direct effect from early maternal PND to offspring depression once the indirect effect via parenting factors was accounted for (B=0.009, 95%CI -0.075, 0.093). Specificity analyses revealed indirect effects through maternal worries about feeding (B=0.019, 95%CI 0.003, 0.035, p=0.010) and maternal perceptions and responses to crying (B=0.018, 95%CI 0.004, 0.032, p=0.012). Conclusions: The adverse impact of maternal PND on offspring depression in early adulthood was explained by maternal nurturing behaviours concerning feeding, crying and sleeping in early childhood. Residual confounding and measurement error likely limit reliable conclusions. If found causal, interventions providing support to reduce worries around maternal nurturing behaviours and treating depression could reduce adverse outcomes in adult offspring of depressed mothers.

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Two functionally redundant FK506-binding proteins regulate multidrug resistance gene expression and govern azole antifungal resistance

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.02415-20 ◽

2021 ◽

Author(s):

Romila Moirangthem ◽

Kundan Kumar ◽

Rupinder Kaur

Keyword(s):

Gene Expression ◽

Binding Proteins ◽

Target Genes ◽

Fungal Infections ◽

Antifungal Resistance ◽

Azole Resistance ◽

Multidrug Resistance Gene ◽

Protein Levels ◽

Fk506 Binding Proteins

Increasing resistance to antifungal therapy is an impediment to effective treatment of fungal infections. Candida glabrata is an opportunistic human fungal pathogen which is inherently less susceptible to cost-effective azole antifungals. Gain-of-function mutations in the Zn-finger pleiotropic drug resistance transcriptional activator-encoding gene, CgPDR1, are the most prevalent cause of azole resistance in clinical settings. CgPDR1 is also transcriptionally activated upon azole exposure, however, factors governing CgPDR1 gene expression are not yet fully understood. Here, we have uncovered a novel role for two FK506-binding proteins, CgFpr3 and CgFpr4, in regulation of the CgPDR1 regulon. We show that CgFpr3 and CgFpr4 possess peptidyl-prolyl isomerase domain, and act redundantly to control CgPDR1 expression, as Cgfpr3Δ4Δ mutant displayed elevated expression of CgPDR1 gene, along with overexpression of its target genes, CgCDR1, CgCDR2 and CgSNQ2, that code for ATP-binding cassette multidrug transporters. Further, CgFpr3 and CgFpr4 are required for maintenance of histone H3 and H4 protein levels, and fluconazole exposure leads to elevated H3 and H4 protein levels. Consistent with a role of histone proteins in azole resistance, disruption of genes coding for the histone demethylase CgRph1 and histone H3K36-specific methyltransferase CgSet2 leads to increased and decreased susceptibility to fluconazole, respectively, with Cgrph1Δ mutant displaying significantly lower basal expression of CgPDR1 and CgCDR1 genes. These data underscore a hitherto unknown role of histone methylation in modulating the most common azole antifungal resistance mechanism. Altogether, our findings establish a link between CgFpr-mediated histone homeostasis and CgPDR1 gene expression, and implicate CgFpr in virulence of C. glabrata.

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Stress-related memories disrupt sociability and associated patterning of hippocampal activity: a role of hilar oxytocin receptor-positive interneurons

Translational Psychiatry ◽

10.1038/s41398-020-01091-y ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Mariah A. A. Meyer ◽

Max Anstötz ◽

Lynn Y. Ren ◽

Michael P. Fiske ◽

Anita L. Guedea ◽

...

Keyword(s):

Oxytocin Receptor ◽

Emotional Behavior ◽

Lateral Septum ◽

Social And Emotional ◽

State Dependent ◽

Affective Symptoms ◽

Traumatic Amnesia ◽

Hippocampal Activity ◽

Cellular Target

AbstractIn susceptible individuals, memories of stressful experiences can give rise to debilitating socio-affective symptoms. This occurs even when the ability to retrieve such memories is limited, as seen in patients suffering from traumatic amnesia. We therefore hypothesized that the encoding, rather than retrieval, mechanisms of stress-related memories underlie their impact on social and emotional behavior. To test this hypothesis, we used combinations of stress-enhanced and state-dependent fear conditioning, which engage different encoding mechanisms for the formation of stress-related memories. We found that the encoding of stress-enhanced state-dependent memories robustly and sex specifically impairs sociability in male mice and disrupts the asymmetry of dentate gyrus (DG)/CA3 activity accompanying social interactions. These deficits were restored by chemogenetic inactivation of oxytocin receptor-positive interneurons localized in the hilus (Oxtr-HI), and by inactivation of dorsohippocampal efferents to the caudal lateral septum. Together, our data suggest that disrupted patterning of dorsohippocampal DG/CA3 activity underlies stress-induced sociability deficits, and that Oxtr-HI can be a cellular target for improving these deficits.

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Συχνότητα των ήπιων νευρολογικών σημείων σε ασθενείς με σχιζοφρενικού τύπου ψύχωση

10.12681/eadd/35462 ◽

2012 ◽

Author(s):

Παναγιώτης Παναγιωτίδης

Keyword(s):

Trait Anxiety ◽

Rating Scale ◽

Depression Scale ◽

Hand Preference ◽

T Test ◽

State Trait Anxiety Inventory ◽

Greek Version ◽

Young Mania ◽

Syndrome Scale ◽

Negative Syndrome

Η παρά τη κλίνη εξέταση των νευρολογικών διαταραχών, μέσω μίας τυπικής νευρολογικής κλινικής εξέτασης θεωρείται ως μία άμεση και ανέξοδη μέθοδος για την αξιολόγηση της εγκεφαλικής δυσλειτουργίας στη σχιζοφρένεια. Κατά τη διάρκεια των τελευταίων σαράντα ετών οι ερευνητικές εργασίες αναφέρουν συστηματικά την αυξημένη παρουσία των ήπιων νευρολογικών σημείων (ΗΝΣ) στους ασθενείς με σχιζοφρένεια, σε σύγκριση με τον υγιή πληθυσμό ή τους μη-ψυχωτικούς ψυχιατρικούς ασθενείς. Ωστόσο, η λειτουργική τους συσχέτιση παραμένει ασαφής και η ειδικότητά τους έχει συχνά αμφισβητηθεί, αν και υπάρχουν ενδείξεις μίας σχετικής ειδικότητας ως προς τη διάγνωση ή τη συμπτωματολογία. Παράγοντες όπως οι ανεπιθύμητες ενέργειες των νευροληπτικών φαρμάκων, το φύλο, η ηλικία ή το οικογενειακό ψυχιατρικό ιστορικό, θεωρείται ότι επηρεάζουν τα αποτελέσματα της νευρολογικής εκτίμησης, ενώ μόνο ένας σχετικά μικρός αριθμός ερευνών αναφέρει δεδομένα μίας μακροχρόνιας παρακολούθησης των ΗΝΣ σε έναν επαρκή αριθμό ατόμων προκειμένου να αξιολογηθεί μία πιθανή έκπτωση των νευρολογικών λειτουργιών. Η παρούσα μελέτη προσπάθησε να διερευνήσει τη συχνότητα και τη φύση των ΗΝΣ σε ασθενείς με σχιζοφρένεια, καθώς και σε μία ομάδα υγιών μαρτύρων. Στοχεύσαμε στη διερεύνηση των διαφορών μεταξύ των μελετώμενων πληθυσμών και των συσχετίσεων μεταξύ συγκεκριμένων ομάδων νευρολογικών σημείων και κλινικών, κοινωνικοδημογραφικών και θεραπευτικών χαρακτηριστικών του πληθυσμού των ασθενών, κατά την αρχική εκτίμηση, καθώς και μετά την πάροδο δώδεκα μηνών. Συνολικά εντάχθηκαν στη μελέτη 133 νοσηλευόμενοι και εξωτερικοί ασθενείς. Οι διαγνώσεις τέθηκαν βάση της ελληνικής έκδοσης 5.0.0. της σύντομης διεθνούς νευροψυχιατρικής συνέντευξης (Mini International Neuropsychiatric Interview, MINI Greek version 5.0.0.). Επιπλέον, 122 υγιείς μάρτυρες συμπεριλήφθηκαν στη μελέτη και αντιστοιχήθηκαν ως προς το φύλο και την ηλικία με τον πληθυσμό των ασθενών. Όλοι οι ενταχθέντες στη μελέτη υποβλήθηκαν αρχικά σε νευρολογική εξέταση εστιασμένη στη διερεύνηση των ΗΝΣ, βάση της Neurological Evaluation Scale (NES) κλίμακας. Τα εξωπυραμιδικά συμπτώματα εκτιμήθηκαν με τις κλίμακες Simpson-Angus Rating Scale (SARS) και Extrapyramidal Symptoms Rating Scale (ESRS). Τα ανευρεθέντα κλινικά συμπτώματα του πληθυσμού της μελέτης αξιολογήθηκαν με τις κλίμακες Positive And Negative Syndrome Scale (PANSS), Calgary Depression Scale for Schizophrenia (CDSS), State-Trait Anxiety Inventory form Y (STAI-T and STAI-S) και Young Mania Rating Scale (YMRS). Τέλος, η εκτίμηση της γενικής λειτουργικότητας έγινε βάση των οδηγιών της Αμερικάνικης Ψυχιατρικής Εταιρείας (κλίμακα GAF), ενώ η προτίμηση χρήσης των χεριών εκτιμήθηκε με την κλίμακα Annett Hand Preference Questionnaire (AHPQ). Για λόγους στατιστικής ανάλυσης υιοθετήθηκε τιμή p τέτοια ώστε να είναι επαρκής για πολλαπλές συγκρίσεις και ορίστηκε σε επίπεδο p<0.001. Για την ανάλυση των δεδομένων χρησιμοποιήθηκε το t-test για ένα δείγμα, η δοκιμασία x2, η δοκιμασία t-test για ανεξάρτητα δείγματα και ο συντελεστής συσχέτισης Pearson, όπου αυτό απαιτείτο. Συμπεράσματα: Τα ήπια νευρολογικά σημεία είναι εξαιρετικά συχνά σε ασθενείς με σχιζοφρένεια (90%), ενώ μάλλον σπάνια σε υγιείς μάρτυρες (12%), εύρημα κοινό σε όλες τις υποομάδες στις οποίες κατηγοριοποιούνται. Η παρουσία τους έχει μορφή δομικών χαρακτηριστικών (trait-like), με σταθερότητα στο χρόνο, και είναι ανεξάρτητα από κοινωνικοδημογραφικούς παράγοντες, κλινικά χαρακτηριστικά της νόσου και την υπάρχουσα φαρμακοθεραπεία, αν και η ύπαρξή τους ενδεχομένως υποδεικνύει νόσο με φτωχότερη έκβαση. Δε φαίνεται να επιδεινώνονται με το πέρασμα της ηλικίας, τουλάχιστον μέχρι την ηλικία των 65 ετών.

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