Etiology Of Psychotic Disorders Research Articles

Нейропсихиатрия: психозы, которые не всегда следует лечить антипсихотиками

Disorders manifested by both neurological and mental disorders belong to the neuropsychiatric diseases. This category includes Alzheimer's disease, Parkinson's disease, Wernicke–Korsakoff syndrome, delirium tremens, catatonia and anti-NMDA receptor encephalitis. The etiology of psychotic disorders in neuropsychiatric diseases probably differs from that in schizophrenia and other psychoses, which causes both inefficiency and adverse events when using antipsychotics in neuropsychiatry. In the absence of a therapeutic alternative, antipsychotics can be prescribed with caution for neurodegenerative disorders, whereas catatonia is a relative, and anti-NMDA receptor encephalitis is an absolute contraindication to their use.

Association in Toxoplasma gondii and Related Psychotic Disorders: A Primary Report.

Implication of infection in etiology of psychotic disorders is an area of interest. We aimed to explore the relationship between Toxoplasma gondii and psychotic disorders in a preliminary study. T. gondii immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies were measured in a sample of patients with psychotic disorders, first-degree relatives (FDR), and healthy volunteers (HV) and compared. Data were analyzed by descriptive statistics in the forms of frequency and percentage using Statistical Package for the Social Sciences (SPSS). Sample size was 10. Men and women were equal. All were from rural background. One patient with psychotic disorder out of the four had anti-T. gondii IgG antibodies in comparison to none among the three each of the FDR and HV. The patient with positive Toxoplasma IgG antibody status had the diagnosis of acute and transient psychotic disorder (ATPD). This pioneering pilot project from this part of the globe highlights a pertinent area for further work in the future in order to have a newer understanding in proper management of psychotic disorder.

Physiological and Pathological Effects of Fetal and Maternal Microchimerism

Microchimerism (Mc) is a bidirectional exchange of fetal and maternal cells during pregnancy. Pregnancy is the most common and natural cause of chimerism. Therefore, we are all born as microchimera. Although there are many unanswered questions it is thought that chimerism has an important role in human health. For many years, the clinical effects of microchimeric cells (McCs) in organ repair and cancer therapy have just begun to be understood. While the mission of chimerism is straight forward, the subject is profound. Chimerism carries the potential for disease as well as for health benefits. This article describes the role of Mc in the etiology of psychotic disorders. In this review, we consider Mc to be a physiological phenomenon, but it can also transform into pathology under inappropriate conditions. We describe in detail below the possible physio-pathological roles of F-MMcCs.

Genetic and psychosocial stressors have independent effects on the level of subclinical psychosis: findings from the multinational EU-GEI study.

Gene x environment (G×E) interactions, i.e. genetic modulation of the sensitivity to environmental factors and/or environmental control of the gene expression, have not been reliably established regarding aetiology of psychotic disorders. Moreover, recent studies have shown associations between the polygenic risk scores for schizophrenia (PRS-SZ) and some risk factors of psychotic disorders, challenging the traditional gene v. environment dichotomy. In the present article, we studied the role of GxE interaction between psychosocial stressors (childhood trauma, stressful life-events, self-reported discrimination experiences and low social capital) and the PRS-SZ on subclinical psychosis in a population-based sample. Data were drawn from the EUropean network of national schizophrenia networks studying Gene-Environment Interactions (EU-GEI) study, in which subjects without psychotic disorders were included in six countries. The sample was restricted to European descendant subjects (n = 706). Subclinical dimensions of psychosis (positive, negative, and depressive) were measured by the Community Assessment of Psychic Experiences (CAPE) scale. Associations between the PRS-SZ and the psychosocial stressors were tested. For each dimension, the interactions between genes and environment were assessed using linear models and comparing explained variances of 'Genetic' models (solely fitted with PRS-SZ), 'Environmental' models (solely fitted with each environmental stressor), 'Independent' models (with PRS-SZ and each environmental factor), and 'Interaction' models (Independent models plus an interaction term between the PRS-SZ and each environmental factor). Likelihood ration tests (LRT) compared the fit of the different models. There were no genes-environment associations. PRS-SZ was associated with positive dimensions (β = 0.092, R2 = 7.50%), and most psychosocial stressors were associated with all three subclinical psychotic dimensions (except social capital and positive dimension). Concerning the positive dimension, Independent models fitted better than Environmental and Genetic models. No significant GxE interaction was observed for any dimension. This study in subjects without psychotic disorders suggests that (i) the aetiological continuum hypothesis could concern particularly the positive dimension of subclinical psychosis, (ii) genetic and environmental factors have independent effects on the level of this positive dimension, (iii) and that interactions between genetic and individual environmental factors could not be identified in this sample.

Risk of first-episode psychosis in migrants to the Republic of Ireland.

Migration is an established risk factor for developing a psychotic disorder in countries with a long history of migration. Less is known for countries with only a recent history of migration. This study aimed to determine the risk for developing a psychotic disorder in migrants to the Republic of Ireland. We included all presentations of first-episode psychosis over 8.5 years to the DETECT Early Intervention for psychosis service in the Republic of Ireland (573 individuals aged 18-65, of whom 22% were first-generation migrants). Psychotic disorder diagnosis relied on SCID. The at-risk population was calculated using census data, and negative binomial regression was used to estimate incidence rate ratios. The annual crude incidence rate for a first-episode psychotic disorder in the total cohort was 25.62 per 100000 population at risk. Migrants from Africa had a nearly twofold increased risk for developing a psychotic disorder compared to those born in the Republic of Ireland (IRR = 1.83, 95% CI 1.11-3.02, p = 0.02). In contrast, migrants from certain Asian countries had a reduced risk, specifically those from China, India, Philippines, Pakistan, Malaysia, Bangladesh and Hong Kong (aIRR = 0.36, 95% CI 0.16-0.81, p = 0.01). Further research into the reasons for this inflated risk in specific migrant groups could produce insights into the aetiology of psychotic disorders. This information should also be used, alongside other data on environmental risk factors that can be determined from census data, to predict the incidence of psychotic disorders and thereby resource services appropriately.

The search for an autoimmune origin of psychotic disorders: Prevalence of autoantibodies against hippocampus antigens, glutamic acid decarboxylase and nuclear antigens

The etiology of psychotic disorders is still unknown, but in a subgroup of patients symptoms might be caused by an autoimmune reaction. In this study, we tested patterns of autoimmune reactivity against potentially novel hippocampal antigens. Serum of a cohort of 621 individuals with psychotic disorders and 257 controls were first tested for reactivity on neuropil of rat brain sections. Brain reactive sera (67 diseased, 27 healthy) were further tested for antibody binding to glutamic acid decarboxylase (GAD) isotype 65 and 67 by cell-based assay (CBA). A sub-cohort of 199 individuals with psychotic disorders and 152 controls was tested for the prevalence of anti-nuclear antibodies (ANA) on HEp2-substrate as well as for reactivity to double-stranded DNA, ribosomal P (RPP), and cardiolipin (CL). Incubation of rat brain with serum resulted in unidentified hippocampal binding patterns in both diseased and control groups. Upon screening with GAD CBA, one of these patterns was identified as GAD65 in one individual with schizophrenia and also in one healthy individual. Two diseased and two healthy individuals had low antibody levels targeting GAD67 by CBA. Antibody reactivity on HEp-2-substrate was increased in patients with schizoaffective disorder, but only in 3 patients did antibody testing hint at a possible diagnosis of systemic lupus erythematosus. Although reactivity of serum to intracellular antigens might be increased in patients with psychotic disorder, no specific targets could be identified. GAD antibodies are very rare and do not seem increased in serum of patients with psychotic disorders.

Natural killer cells in first-episode psychosis: an innate immune signature?

Accumulating evidence majorly implicates immune dysfunction in the etiology of psychotic disorders. In particular, altered numbers and functions of natural killer (NK) cells have been described in psychosis, but interpretation has often been confounded by a number of biases, including treatment. Eighty-one first-episode psychosis (FEP) patients who subsequently received a diagnosis of either schizophrenia (SZ; n = 30) or bipolar disorder (BP; n = 31) over a five-year follow-up period were investigated for their NK cell phenotype and compared to 61 healthy controls (HCs). We found a similar proportion of CD3-CD56+ NK cells in FEP patients and HCs. The frequency of NK cells expressing the late cell activation marker HLA-DR was significantly increased in FEP patients compared to HCs, especially in patients with BP (p < 0.0001) and, to a lesser degree, in patients with SZ (p = 0.0128). Interestingly, the expression of the activating NKG2C receptor, known to be associated with infections, was higher in patients with SZ and BP than in HCs (p < 0.0001) and correlated with HLA-DR expression, altogether defining adaptive NK cells. In terms of NK cell function, we observed a suppressed capacity of SZ-derived NK cells to mount cytotoxic responses in the presence of target cells, while NK cells from patients with BP show an inability to produce IFN-γ, a cytokine pivotal to NK function. This study strongly suggests major dysfunction of NK cells in FEP with functioning impairment correlated with psychotic, manic, and depressive symptoms in subsequently diagnosed patients with SZ and BP.

Overview of Schizophrenia and Other Psychotic Disorders

Psychotic disorders are among the most disabling conditions and constitute a major public health problem. Described throughout recorded time, they affect as many as 5% of the population and cause a disproportionate amount of suffering and loss to society. In the chapter on schizophrenia spectrum and other psychotic disorders, the DSM-5 lists delusional disorder, brief psychotic disorder, schizophreniform disorder, schizophrenia, and schizoaffective disorder, as well as categories for substance- or medically induced psychotic disorders. The term psychosis indicates that the individual has a severe inability to interpret the surrounding environment in a realistic way. Symptoms include hallucinations, delusions, and bizarre behavior. Psychotic disorders are associated with premature death, mostly attributable to suicide. The pathophysiology and etiology of psychotic disorders are only now beginning to be understood, and treatment for these conditions remains suboptimal. Researchers are currently refining the cause of these symptoms and developing more effective treatments. This review contains 3 tables, and 34 references. Key words: Brief psychotic disorder, delusions, hallucinations, psychosis, schizoaffective disorder, schizophrenia, schizophreniform disorder

Overview of Schizophrenia and Other Psychotic Disorders

Psychotic disorders are among the most disabling conditions and constitute a major public health problem. Described throughout recorded time, they affect as many as 5% of the population and cause a disproportionate amount of suffering and loss to society. In the chapter on schizophrenia spectrum and other psychotic disorders, the DSM-5 lists delusional disorder, brief psychotic disorder, schizophreniform disorder, schizophrenia, and schizoaffective disorder, as well as categories for substance- or medically induced psychotic disorders. The term psychosis indicates that the individual has a severe inability to interpret the surrounding environment in a realistic way. Symptoms include hallucinations, delusions, and bizarre behavior. Psychotic disorders are associated with premature death, mostly attributable to suicide. The pathophysiology and etiology of psychotic disorders are only now beginning to be understood, and treatment for these conditions remains suboptimal. Researchers are currently refining the cause of these symptoms and developing more effective treatments. This review contains 3 tables, and 34 references. Key words: Brief psychotic disorder, delusions, hallucinations, psychosis, schizoaffective disorder, schizophrenia, schizophreniform disorder

Overview of Schizophrenia and Other Psychotic Disorders

Psychotic disorders are among the most disabling conditions and constitute a major public health problem. Described throughout recorded time, they affect as many as 5% of the population and cause a disproportionate amount of suffering and loss to society. In the chapter on schizophrenia spectrum and other psychotic disorders, the DSM-5 lists delusional disorder, brief psychotic disorder, schizophreniform disorder, schizophrenia, and schizoaffective disorder, as well as categories for substance- or medically induced psychotic disorders. The term psychosis indicates that the individual has a severe inability to interpret the surrounding environment in a realistic way. Symptoms include hallucinations, delusions, and bizarre behavior. Psychotic disorders are associated with premature death, mostly attributable to suicide. The pathophysiology and etiology of psychotic disorders are only now beginning to be understood, and treatment for these conditions remains suboptimal. Researchers are currently refining the cause of these symptoms and developing more effective treatments. This review contains 3 tables, and 34 references. Key words: Brief psychotic disorder, delusions, hallucinations, psychosis, schizoaffective disorder, schizophrenia, schizophreniform disorder

Overview of Schizophrenia and Other Psychotic Disorders

Psychotic disorders are among the most disabling conditions and constitute a major public health problem. Described throughout recorded time, they affect as many as 5% of the population and cause a disproportionate amount of suffering and loss to society. In the chapter on schizophrenia spectrum and other psychotic disorders, the DSM-5 lists delusional disorder, brief psychotic disorder, schizophreniform disorder, schizophrenia, and schizoaffective disorder, as well as categories for substance- or medically induced psychotic disorders. The term psychosis indicates that the individual has a severe inability to interpret the surrounding environment in a realistic way. Symptoms include hallucinations, delusions, and bizarre behavior. Psychotic disorders are associated with premature death, mostly attributable to suicide. The pathophysiology and etiology of psychotic disorders are only now beginning to be understood, and treatment for these conditions remains suboptimal. Researchers are currently refining the cause of these symptoms and developing more effective treatments. This review contains 3 tables, and 34 references. Key words: Brief psychotic disorder, delusions, hallucinations, psychosis, schizoaffective disorder, schizophrenia, schizophreniform disorder

T157. FRONTOSTRIATAL CONNECTIVITY IN TREATMENT-RESISTANT SCHIZOPHRENIA: RELATIONSHIP TO POSITIVE SYMPTOMS AND COGNITIVE FLEXIBILITY

BackgroundThe frontostriatal circuits linking different parts of the frontal cortex to subregions of the striatum are proposed to regulate different aspects of cognition, executive function, affect and reward processing. Dysregulation of these brain circuits is also known to be important in the etiology of psychotic disorders, with the magnitude of dysfunction correlating with the severity of positive symptoms. These observations suggest that the integrity of brain circuits connected to the striatum is important for antipsychotic treatment response as well as specific cognitive processes. However, not all individuals with schizophrenia benefit from antipsychotic treatment, with up to 20% of individuals considered to be treatment-resistant. These individuals also show pervasive impairments in cognition, including cognitive flexibility. Nevertheless, few studies have examined striatal connectivity in treatment-resistant schizophrenia (TRS), particularly in relation to positive symptomatology and specific cognitive deficits subserved by the striatal circuits. This study therefore aimed to (i) assess for disruptions in frontostriatal connectivity in a sample of TRS and (ii) assess the relationship between the frontostriatal circuits with positive symptoms and attentional set-shifting (cognitive flexibility) given recent associations with the dorsal striatal circuit.MethodsResting-state functional magnetic resonance imaging was used to investigate functional connectivity (FC) in 42 TRS participants prescribed clozapine (30 males, mean age=41.3(10)), and 42 healthy controls (24 males, mean age=38.4(10)). The whole striatum (caudate, putamen and nucleus accumbens) and the left and right dorsal striatum were separately seeded as regions of interest, and Pearson’s correlations between the seeds and all other voxels comprising cortical and subcortical gray matter were investigated. For brain regions that showed significant group differences in FC with the striatal seeds, Pearson’s correlations explored the relationship between the strength of connectivity with positive symptoms and attentional set-shifting (extradimensional shift errors) as measured with the CANTAB intra-/extradimensional set shift task.ResultsIn comparison with healthy controls, TRS patients displayed significantly reduced FC between the whole striatum and the bilateral anterior cingulate, cerebellum, precuneus, right and left frontal pole and left insular/temporal pole, and reduced FC of the left and right dorsal striatum with cerebellum, and between the right dorsal striatum and bilateral cingulate and right frontal pole. Reduced FC between the whole striatum and precuneus and insular/temporal pole was associated with greater delusions of jealousy (p<.002 uncorrected); no other associations with positive symptoms were detected. In the entire sample, reduced FC from all striatal seeds was associated with greater extradimensional errors, indicating worse cognitive flexibility. These associations were not detected in TRS and controls separately.DiscussionOur preliminary findings reveal reduced striatal FC in TRS, including hypoconnectivity of the dorsal striatal circuit. In contrast to early psychosis, reduced dorsal striatal connectivity does not appear to mediate positive symptoms. Our finding relating hypoconnectivity of the striatal circuits with impaired cognitive flexibility is partly consistent with recent observations in other psychiatric disorders, although such deficits appear not specific to the dorsal circuit and to TRS. Future work will examine connectivity of the ventral striatum, as well as striatal connectivity in early-onset psychosis and siblings of patients with schizophrenia.

Sun Exposure and Psychotic Experiences.

Sun exposure is considered the single most important source of vitamin D. Vitamin D deficiency has been suggested to play a role in the etiology of psychotic disorders. The aim of the present study was to evaluate the association between sun exposure and psychotic experiences (PEs) in a general population sample of Swedish women. The study population included participants from The Swedish Women's Lifestyle and Health cohort study. The 20-item community assessment of psychic experiences (CAPEs) was administered between ages 30 and 50 to establish PEs. Sun exposure as measured by (1) sunbathing holidays and (2) history of sunburn was measured between ages 10 and 39. The association between sun exposure and PEs was evaluated by quantile regression models. 34,297 women were included in the analysis. Women who reported no sunbathing holidays and 2 or more weeks of sunbathing holidays scored higher on the CAPE scale than women exposed to 1 week of sunbathing holidays across the entire distribution, when adjusting for age and education. Similarly, compared with women who reported a history of one sunburn, the women with none or two or more sunburns showed higher scores on the CAPE scale. The results of the present study suggest that, in a population-based cohort of middle aged women, both low and high sun exposure is associated with increased level of positive PEs.

Impact of vulnerability to stress in the development and course of first psychotic episode

IntroductionThe stress diathesis hypothesis is one of the leading models of etiology of psychotic disorders. Cortisol is one of the most researched stress hormone; yet its role in first psychotic episode is currently subject of many researches. Psychotic disorder occurs when “enough” stress attacks vulnerable personality. Stress response activates HPA axis that results in cascade effects on several body systems (immune, neuroendocrine and inflammatory). Dysregulation of the HPA axis and increased cortisol levels have been implicated in psychotic as well as in other psychiatric disorders.ObjectiveTo follow treatment response through changes in clinical status and stress biomarkers evaluation in longitudinal 18 months research in drug naive FEP.AimTo assess endocrine and autonomic responses to acute psychosocial stress, their associations with onset of the first psychotic episode and their subsequent remission.MethodsWe studied 17 subjects with FEP and age and gender matched controls who were exposed to the Trier Social Stress Test. Other materials have explored clinical status through standardized clinical psychiatric interview and validated psychiatry scales as well as measured laboratory biomarkers (cortisol, prolactin, insulin).ResultsOur preliminary findings on a sample of 40 participants indicate a differences between patients and controls in terms of response to stress measured by TSST.ConclusionIn our continued longitudinal research, we plan to further explore the role of hypothalamic-pituitary-adrenal activity in onset and course of psychotic disorder and its relation with other biomarkers.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Social Stress and Psychosis Risk: Common Neurochemical Substrates?

Environmental risk factors have been implicated in the etiology of psychotic disorders, with growing evidence showing the adverse effects of migration, social marginalization, urbanicity, childhood trauma, social defeat, and other adverse experiences on mental health in vulnerable populations. Collectively, social stress may be one mechanism that could link these environmental risk factors. The exact mechanism(s) by which social stress can affect brain function, and in particular the molecular targets involved in psychosis (such as the dopaminergic (DA) system), is (are) not fully understood. In this review, we will discuss the interplay between social environmental risk factors and molecular changes in the human brain; in particular, we will highlight the impact of social stress on three specific neurochemical systems: DA, neuroinflammation/immune, and endocannabinoid (eCB) signaling. We have chosen the latter two molecular pathways based on emerging evidence linking schizophrenia to altered neuroinflammatory processes and cannabis use. We further identify key developmental periods in which social stress interacts with these pathways, suggesting window(s) of opportunities for novel interventions. Taken together, we suggest that they may have a key role in the pathogenesis and disease progression, possibly provide novel treatment options for schizophrenia, and perhaps even prevent it.

A population-based study of the risk of schizophrenia and bipolar disorder associated with parent-child separation during development.

There is growing interest in the role of childhood adversities, including parental death and separation, in the etiology of psychotic disorders. However, few studies have used prospectively collected data to specifically investigate parental separation across development, or assessed the importance of duration of separation, and family characteristics. We measured three types of separation not due to death: maternal, paternal, and from both parents, across the ages of 1-15 years among a cohort of 985 058 individuals born in Denmark 1971-1991 and followed to 2011. Associations with narrowly and broadly defined schizophrenia and bipolar disorder in the psychiatric register were assessed in terms of separation occurrence, age of separation, and number of years separated. Interactions with parental history of mental disorder were assessed. Each type of separation was associated with all three outcomes, adjusting for age, sex, birth period, calendar year, family history of mental disorder, urbanicity at birth and parental age. Number of years of paternal separation was positively associated with both schizophrenia and bipolar disorder. Associations between separation from both parents and schizophrenia were stronger when separation occurred at later ages, while those with bipolar disorder remained stable across development. The first occurrence of paternal separation appeared to increase risk more when it occurred earlier in childhood. Associations differed according to parental history of mental disorder, although in no situation was separation protective. Effects of parental separation may differ by type, developmental timing and family characteristics. These findings highlight the importance of considering such factors in studies of childhood adversity.

Epigenetic mechanisms in the pathophysiology of psychotic disorders.

Epigenetics is the study of chromatin-the physical material that forms chromosomes, composed of DNA wound around specialized histone proteins-and of how the modification of chromatin acts to establish stable states of gene expression in a cell-specific manner. Chromatin is regulated through three mechanisms: DNA methylation, histone modification, and RNA interference. These basic biological processes form the molecular interface between the genome and the environment, contributing to the regulation of gene expression in health and disease. Investigation of epigenetic mechanisms is yielding exciting insights in many areas of medicine, and a large and rapidly growing literature describes epigenetics as central to many aspects of the pathophysiology of psychotic disorders. This article first discusses speculative points as to why the mechanisms of epigenetics may be satisfying explanatory mechanisms in the etiology of psychotic disorders, then details emerging experimental evidence of roles for the three types of epigenetic mechanisms in these illnesses, and finally discusses these mechanisms as potentially compelling areas of research for the development of future treatments.

Cerebellar-motor dysfunction in schizophrenia and psychosis-risk: the importance of regional cerebellar analysis approaches.

Motor abnormalities in individuals with schizophrenia and those at-risk for psychosis are well documented. An accumulating body of work has also highlighted motor abnormalities related to cerebellar dysfunction in schizophrenia including eye-blink conditioning, timing, postural control, and motor learning. We have also recently found evidence for motor dysfunction in individuals at ultra high-risk for psychosis (1–3). This is particularly relevant as the cerebellum is thought to be central to the cognitive dysmetria model of schizophrenia, and these overt motor signs may point to more general cerebellar dysfunction in the etiology of psychotic disorders. While studies have provided evidence indicative of motor cerebellar dysfunction in at-risk populations and in schizophrenia, findings with respect to the cerebellum have been mixed. One factor potentially contributing to these mixed results is the whole-structure approach taken when investigating the cerebellum. In non-human primates, there are distinct closed-loop circuits between the cerebellum, thalamus, and brain with motor and non-motor cortical regions. Recent human neuroimaging has supported this finding and indicates that there is a cerebellar functional topography (4), and this information is being missed with whole-structure approaches. Here, we review cerebellar-motor dysfunction in individuals with schizophrenia and those at-risk for psychosis. We also discuss cerebellar abnormalities in psychosis, and the cerebellar functional topography. Because of the segregated functional regions of the cerebellum, we propose that it is important to look at the structure regionally in order to better understand its role in motor dysfunction in these populations. This is analogous to approaches taken with the basal ganglia, where each region is considered separately. Such an approach is necessary to better understand cerebellar pathophysiology on a macro-structural level with respect to the pathogenesis of psychosis.

Common versus psychopathology-specific risk factors for psychotic experiences and depression during adolescence.

An argument often used to support the view that psychotic experiences (PEs) in general population samples are a valid phenotype for studying the aetiology of schizophrenia is that risk factors for schizophrenia show similar patterns of association with PEs. However, PEs often co-occur with depression, and no study has explicitly tested whether risk factors for schizophrenia are shared between PEs and depression, or are psychopathology specific, while jointly modelling both outcomes. We used data from 7030 subjects from a birth cohort study. Depression and PEs at age 18 years were assessed using self-report questionnaires and semi-structured interviews. We compared the extent to which risk factors for schizophrenia across sociodemographic, familial, neurodevelopmental, stress-adversity, emotional-behavioural and substance use domains showed different associations with PEs and depression within bivariate models that allowed for their correlation. Most of the exposures examined were associated, to a similar degree, with an increased risk of both outcomes. However, whereas female sex and family history of depression showed some discrimination as potential risk factors for depression and PEs, with stronger associations in the former, markers of abnormal neurodevelopment showed stronger associations with PEs. The argument that PEs are valid markers for studying the aetiology of schizophrenia, made simply on the basis that they share risk factors in common, is not well supported. PEs seem to be a weak index of genetic and environmental risk for schizophrenia; however, studies disentangling aetiological pathways to PEs from those impacting upon co-morbid psychopathology might provide important insights into the aetiology of psychotic disorders.

Is catechol-o-methyltransferase gene polymorphism a risk factor in the development of premenstrual syndrome?

ObjectiveThe objective of this study was to investigate whether there was a correlation between catechol-o-methyltransferase (COMT) gene polymorphism, which is believed to play a role in the etiology of psychotic disorders, and premenstrual syndrome (PMS).MethodsFifty-three women with regular menstrual cycles, aged between 18 and 46 years and diagnosed with PMS according to the American Congress of Obstetrics and Gynecology criteria were included in this study as the study group, and 53 healthy women having no health problems were selected as the controls. Venous blood was collected from all patients included in the study and kept at -18℃ prior to analysis.ResultsThere was no significant difference between the groups in terms of demographic features such as age, body mass index, number of pregnancies, parity, and number of children. No statistically significant difference was observed in terms of COMT gene polymorphism (p=0.61) between women in the PMS and the control groups. However, a significant difference was found between arthralgia, which is an indicator of PMS, and low-enzyme activity COMT gene (Met/Met) polymorphism (p=0.04).ConclusionThese results suggested that there was no significant relationship between PMS and COMT gene polymorphism. Since we could not find a direct correlation between the COMT gene polymorphism and PMS, further studies including alternative neurotransmitter pathways are needed to find an effective treatment for this disease.