Prenatal and perinatal risk and protective factors for psychosis: a systematic review and meta-analysis

Davies, Cathy; Segre, Giulia; Estradé, Andrés; Raduà, Joaquim; Micheli, Andrea De; Provenzani, Umberto; Oliver, Dominic; Pablo, Gonzalo Salazar de; Ramella-Cravaro, Valentina; Besozzi, Maria; Dazzan, Paola; Miele, Maddalena; Caputo, Gianluigi; Spallarossa, Cecilia; Crossland, Georgia; Ilyas, Athif; Spada, Giulia; Politi, Pierluigi; Murray, Robin M.; McGuire, Philip; Fusar‐Poli, Paolo

doi:10.1016/s2215-0366(20)30057-2

Cited by 198 publications

(169 citation statements)

References 84 publications

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“…Recent studies have focused on sex differences in psychopathologic outcomes associated with PS including anxiety, depression, ADHD, schizophrenia, and autism (Weinstock, 2001;Walsh et al, 2019;Davies et al, 2020;Scheinost et al, 2020). Chronic maternal stress was shown to increase anxiety-and depression-like behavior in prepubertal males relative to controls, whereas prepubertal females were less affected (Schulz et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Differences in DNA Methylation Reprogramming Underlie the Sexual Dimorphism of Behavioral Disorder Caused by Prenatal Stress in Rats

Lei

et al. 2020

Front. Neurosci.

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Prenatal stress (PS) can lead to neuroendocrine and emotional disorders later in adolescence. Sexual dimorphism in these neurodevelopmental outcomes have been observed; however, the underlying mechanisms are not fully understood. To address this issue, we investigated whether there are sex differences in epigenetic reprogramming in rats exposed to PS. Pregnant female rats were subjected to chronic restraint stress from gestational day (G)12 to G18. From postnatal day (P)38 to P45, subgroups of offspring including both males and females were subjected to behavioral testing and brain tissue specimens were analyzed by DNA pyrosequencing, western blotting, and Golgi staining to assess changes in methylation pattern of glucocorticoid receptor (GR) gene, expression of DNA methyltransferase (DNMT) and DNA demethylase, and dendrite morphology, respectively. The DNA methyltransferase inhibitor decitabine was administered to rats prior to PS to further evaluate the role of methylation in the sexually dimorphic effects of PS. The results showed that PS increased anxiety-like behavior in offspring, especially in females, while depression-like behavior was increased in male offspring compared to control littermates. The methylation pattern in the promoter region of the GR gene differed between males and females. Sex-specific changes in the expression of DNMTs (DNMT1 and DNMT3a) and DNA demethylase (Tet methylcytosine dioxygenase 2) were also observed. Interestingly, decitabine alleviated the behavioral disorder caused by PS and restored dendrite density and morphology in female but not male rats. These findings suggest that different change patterns of DNMT and demethylase in the two sexes after PS are responsible for the sexually dimorphism, which could have implications for the clinical management of stress-related disorders.

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Section: Discussionmentioning

confidence: 99%

Differences in DNA Methylation Reprogramming Underlie the Sexual Dimorphism of Behavioral Disorder Caused by Prenatal Stress in Rats

Lei

et al. 2020

Front. Neurosci.

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“…Genome wide association studies have also shown an increase in risk related to single nucleotide polymorphisms in oligodendrocyte specific genes ( 42 ). Furthermore, rodent models have shown that 2 nd trimester insults, especially maternal infection, a known risk factor for schizophrenia ( 43 ), can produce a decrease in fractional anisotropy (FA) in fronto-striatal-limbic circuitry similar to that seen in the illness ( 44 ). Supporting these discoveries, investigators have characterized white matter abnormalities in the CHR population.…”

Section: Structural Phenotypesmentioning

confidence: 99%

“…Inflammation has long been associated with the pathophysiology of schizophrenia ( 75 ). Winter births and maternal infections ( 43 ), genetic risk associated with the major histocompatibility complex ( 76 ), and subsequent discovery of the association of complement protein C4A ( 77 ) all represent converging evidence for the involvement of inflammation in the disease. Furthermore, in CHR subjects, several lines of evidence indicate increased inflammation prior to first episode psychosis.…”

Section: Inflammatory Phenotypesmentioning

confidence: 99%

Selective Review of Neuroimaging Findings in Youth at Clinical High Risk for Psychosis: On the Path to Biomarkers for Conversion

2020

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First episode psychosis (FEP), and subsequent diagnosis of schizophrenia or schizoaffective disorder, predominantly occurs during late adolescence, is accompanied by a significant decline in function and represents a traumatic experience for patients and families alike. Prior to first episode psychosis, most patients experience a prodromal period of 1–2 years, during which symptoms first appear and then progress. During that time period, subjects are referred to as being at Clinical High Risk (CHR), as a prodromal period can only be designated in hindsight in those who convert. The clinical high-risk period represents a critical window during which interventions may be targeted to slow or prevent conversion to psychosis. However, only one third of subjects at clinical high risk will convert to psychosis and receive a formal diagnosis of a primary psychotic disorder. Therefore, in order for targeted interventions to be developed and applied, predicting who among this population will convert is of critical importance. To date, a variety of neuroimaging modalities have identified numerous differences between CHR subjects and healthy controls. However, complicating attempts at predicting conversion are increasingly recognized co-morbidities, such as major depressive disorder, in a significant number of CHR subjects. The result of this is that phenotypes discovered between CHR subjects and healthy controls are likely non-specific to psychosis and generalized for major mental illness. In this paper, we selectively review evidence for neuroimaging phenotypes in CHR subjects who later converted to psychosis. We then evaluate the recent landscape of machine learning as it relates to neuroimaging phenotypes in predicting conversion to psychosis.

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“…Even if SSD and ASD are currently considered distinct entities, they both represent chronic, multi-factorial disorders. They share genetic predispositions [10,11] and environmental risk factors, such as complications during pregnancy or at birth [12,13]. Moreover, they present with similar neuroimaging patterns [14,15], neurochemical abnormalities, such as dopaminergic dysregulations [16,17], and inflammatory pathways [18].…”

Section: Introductionmentioning

confidence: 99%

Self-Reported Autistic Traits Using the AQ: A Comparison between Individuals with ASD, Psychosis, and Non-Clinical Controls

et al. 2020

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The term “autism” was originally coined by Eugen Bleuler to describe one of the core symptoms of schizophrenia. Even if autism spectrum disorder (ASD) and schizophrenia spectrum disorders (SSD) are now considered two distinct conditions, they share some clinical features. The present study aimed to investigate self-reported autistic traits in individuals with ASD, SSD, and non-clinical controls (NCC), using the Autism-Spectrum Quotient (AQ), a 50-item questionnaire. The study was conducted in the Psychiatry Unit of Policlinico “G. Rodolico”, Catania, Italy. The AQ was administered to 35 adults with ASD, 64 with SSD, and 198 NCC. Overall, our data showed that the ASD sample scored significantly higher than NCC. However, no significant differences were detected between individuals with ASD and SSD. Notably, the three groups scored similarly in the subscale “attention to detail”. AQ showed good accuracy in differentiating ASD from NCC (AUC = 0.84), while discriminant ability was poor in the clinical sample (AUC = 0.63). Finally, AQ did not correlate with clinician-rated ADOS-2 scores in the ASD sample. Our study confirms that symptoms are partially overlapping in adults with ASD and psychosis. Moreover, they raise concerns regarding the usefulness of AQ as a screening tool in clinical populations.

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Prenatal and perinatal risk and protective factors for psychosis: a systematic review and meta-analysis

Cited by 198 publications

References 84 publications

Differences in DNA Methylation Reprogramming Underlie the Sexual Dimorphism of Behavioral Disorder Caused by Prenatal Stress in Rats

Differences in DNA Methylation Reprogramming Underlie the Sexual Dimorphism of Behavioral Disorder Caused by Prenatal Stress in Rats

Selective Review of Neuroimaging Findings in Youth at Clinical High Risk for Psychosis: On the Path to Biomarkers for Conversion

Self-Reported Autistic Traits Using the AQ: A Comparison between Individuals with ASD, Psychosis, and Non-Clinical Controls

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