Schizophrenia is a neuropsychiatric disorder characterized by dissociation of thoughts, idea, identity, and emotions. It has no central pathophysiological mechanism and precise diagnostic markers. Despite its high heritability, there are also environmental factors implicated in the development of schizophrenia. Epigenetic factors are thought to mediate the effects of environmental factors in the development of the disorder. Epigenetic modifications like DNA methylation are a risk factor for schizophrenia. Targeted gene approach studies attempted to find candidate gene methylation, but the results are contradictory. Genome-wide methylation studies are insufficient in literature and the available data do not cover different populations like the African populations. The current genome-wide studies have limitations related to the sample and methods used. Studies are required to control for these limitations. Integration of DNA methylation, gene expression, and their effects are important in the understanding of the development of schizophrenia and search for biomarkers. There are currently no precise and functional biomarkers for the disorder. Several epigenetic markers have been reported to be common in functional and peripheral tissue. This makes the peripheral tissue epigenetic changes a surrogate of functional tissue, suggesting common epigenetic alteration can be used as biomarkers of schizophrenia in peripheral tissue.
Advances in our understanding of the genetics of mental disorders (MD) have contributed to a better understanding of their pathophysiology. Nonetheless, several questions and doubts remain. Recent research has focused on the role of the environment in developing mental disorders, and the advent of neuroscientific methodologies has opened up new avenues of inquiry. However, the mechanism by which childhood stress affects neurodevelopment via mechanisms, such as gene-environment interactions and epigenetic regulation leading to diseases in adulthood, is unclear. This paper aims to review the evidence on the role of early life stress and parental psychopathology in the pathophysiology and clinical expression of MD. Methodology: The study will conduct a comprehensive systematic review using medical search terms (MeSH). Electronic searches for published studies will be performed using the MEDLINE (PubMed), EMBASE, Scopus, PsychINFO, Web of Science, and Google Scholar databases. We will look for research on the neuroplasticity effects of early life stress on development and review articles that evaluate cognitive functions and the development of psychopathology and MD. Before identifying full-text articles, several studies will be filtered based on titles, abstracts, keywords, and synonyms. Publications to be included in the review will be assessed for quality and consistency before inclusion. Data will be extracted independently and duplicated by two authors from each eligible study to ensure consistency between reviews. All databases will be searched from inception until July 2021 and will be limited to human studies. The search will be limited only to publication in the English language and any publication that can be converted to English. Discussion and Conclusions: The findings of this review will meticulously articulate the effects of childhood adversity, such as ELS and parental psychopathology on cognitive development and neuroplasticity.
Background: Schizophrenia is a heterogeneous neuropsychiatric disorder, categorized by positive, negative, and cognitive symptoms. In trying to improve the diagnosis and treatment of schizophrenia, researchers have turned to “dual hit” models of schizophrenia that are able to reproduce all symptoms of the disorder. The main objective of this protocol is to present a transparent process on how we plan to review the existing international literature on the effectiveness of “dual hit” models used to induce schizophrenia on rodents. Methods: Literature search strategies will be developed using medical search headings (MeSH). The MEDLINE (PubMed), EMBASE, and Google Scholar databases will be used to search for electronically published studies. We will search for studies involving inducing schizophrenic symptoms using “dual hit” rodent models (post-weaning social isolation and NMDA receptor antagonist). Studies will be screened by titles, abstracts, keywords, and synonyms followed by identifying the full-text articles. All studies that will pass quality assessment will be included. Data will be extracted by two authors independently and in duplicate from each eligible study to ensure that there is consistency between reviews. If the design and comparator are sufficiently homogenous for all studies, a meta-analysis will be conducted using a random-effect model. Discussion: The results of this review will contribute to the development of new “dual hit” models that will be able to characterize schizophrenia symptoms better. It will also shed light to researchers on new developments that need to be made in improving animal models of schizophrenia.
BackgroundSchizophrenia is a heterogeneous neuropsychiatric disorder, categorized by positive, negative, and cognitive symptoms. In trying to improve diagnosis and treatment of schizophrenia researchers have turn to “dual hit” models of schizophrenia that are able to reproduce all symptoms of the disorder. The main objective of this protocol is to present a transparent process on how we plan to review the existing international literature on effectiveness of “dual hit” models used to induce schizophrenia on rodents. MethodsLiterature search strategies will be developed using medical search headings (MeSH). The MEDLINE (PubMed), EMBASE, and Google Scholar databases will be used to search for published studies electronically. We will search for studies involving inducing schizophrenic symptoms using “dual hit” rodent model (post-weaning social isolation and NMDA receptor antagonist). Studies will be screened by titles, abstracts, keywords, and synonyms followed by identifying the full-text articles. All studies that will pass the quality assessment will be included. Data will be extracted by two authors independently and in duplicate, from each eligible study in ensuring that there is consistency between reviews. If the design and comparator are sufficiently homogenous for all studies, meta-analysis will be conducted using a random-effect model.DiscussionThe results of this review will contribute in the development of new “dual hit” models that will be able to characterize schizophrenia symptoms better. It will also shed light to researchers on new developments that need to be made in improving animal models of schizophrenia.Systematic reviews registrationPROSPERO CRD42021247585
Schizophrenia is a debilitating psychiatric disorder comprising positive, negative, and cognitive impairments. Most of the animal models developed to understand the neurobiology and mechanism of schizophrenia do not produce all the symptoms of the disease. Therefore, researchers need to develop new animal models with greater translational reliability, and the ability to produce most if not all symptoms of schizophrenia. This review aimed to evaluate the effectiveness of the rodent “double hit” (post-weaning social isolation and N-methyl-D-aspartate (NMDA) receptor antagonist) model to produce symptoms of schizophrenia. This systematic review was developed according to the 2020 PRISMA guidelines and checklist. The MEDLINE (PubMed) and Ebscohost databases were used to search for studies. The systematic review is based on quantitative animal studies. Studies in languages other than English that could be translated sufficiently using Google translate were also included. Data extraction was performed individually by two independent reviewers and discrepancies between them were resolved by a third reviewer. SYRCLE’s risk-of-bias tool was used to test the quality and biases of included studies. Our primary search yielded a total of 47 articles, through different study selection processes. Seventeen articles met the inclusion criteria for this systematic review. Ten of the seventeen studies found that the “double hit” model was more effective in developing various symptoms of schizophrenia. Most studies showed that the “double hit” model is robust and capable of inducing cognitive impairments and positive symptoms of schizophrenia.
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