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      Involvement of the Expression of G Protein-Coupled Receptors in Schizophrenia

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      Pharmaceuticals

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          Abstract

          The expression of GPCRs has been associated with schizophrenia, and their expression may induce morphological changes in brain regions responsible for schizophrenia and disease-specific behavioral changes. The articles included in this review were selected using keywords and databases of scientific research websites. The expressions of GPRs have different involvements in schizophrenia, some increase the risk while others provide protection, and they may also be potential targets for new treatments. Proper evaluation of these factors is essential to have a better therapeutic response with a lower rate of chronicity and thus improve the long-term prognosis.

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          Schizophrenia, Dopamine and the Striatum: From Biology to Symptoms

          The mesolimbic hypothesis has been a central dogma of schizophrenia for decades, positing that aberrant functioning of midbrain dopamine projections to limbic regions causes psychotic symptoms. Recently, however, advances in neuroimaging techniques have led to the unanticipated finding that dopaminergic dysfunction in schizophrenia is greatest within nigrostriatal pathways, implicating the dorsal striatum in the pathophysiology and calling into question the mesolimbic theory. At the same time our knowledge of striatal anatomy and function has progressed, suggesting new mechanisms via which striatal dysfunction may contribute to the symptoms of schizophrenia. This Review draws together these developments, to explore what they mean for our understanding of the pathophysiology, clinical manifestations, and treatment of the disorder.
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            Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies.

            There are many published twin studies of schizophrenia. Although these studies have been reviewed previously, to our knowledge, no review has provided quantitative summary estimates of the impact of genes and environment on liability to schizophrenia that also accounted for the different ascertainment strategies used. To calculate meta-analytic estimates of heritability in liability and shared and individual-specific environmental effects from the pooled twin data. We used a structured literature search to identify all published twin studies of schizophrenia, including MEDLINE, dissertation, and books-in-print searches. Of the 14 identified studies, 12 met the minimal inclusion criteria of systematic ascertainment. By using a multigroup twin model, we found evidence for substantial additive genetic effects-the point estimate of heritability in liability to schizophrenia was 81% (95% confidence interval, 73%-90%). Notably, there was consistent evidence across these studies for common or shared environmental influences on liability to schizophrenia-joint estimate, 11% (95% confidence interval, 3%-19%). Despite evidence of heterogeneity across studies, these meta-analytic results from 12 published twin studies of schizophrenia are consistent with a view of schizophrenia as a complex trait that results from genetic and environmental etiological influences. These results are broadly informative in that they provide no information about the specific identity of these etiological influences, but they do provide a component of a unifying empirical basis supporting the rationality of searches for underlying genetic and common environmental etiological factors.
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              Hippocampal dysfunction in the pathophysiology of schizophrenia: a selective review and hypothesis for early detection and intervention

              Scientists have long sought to characterize the pathophysiologic basis of schizophrenia and develop biomarkers that could identify the illness. Extensive postmortem and in vivo neuroimaging research has described the early involvement of the hippocampus in the pathophysiology of schizophrenia. In this context, we have developed a hypothesis that describes the evolution of schizophrenia—from the premorbid through the prodromal stages to syndromal psychosis—and posits dysregulation of glutamate neurotransmission beginning in the CA1 region of the hippocampus as inducing attenuated psychotic symptoms and initiating the transition to syndromal psychosis. As the illness progresses, this pathological process expands to other regions of the hippocampal circuit and projection fields in other anatomic areas including the frontal cortex, and induces an atrophic process in which hippocampal neuropil is reduced and interneurons are lost. This paper will describe the studies of our group and other investigators supporting this pathophysiological hypothesis, as well as its implications for early detection and therapeutic intervention.
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                Author and article information

                Contributors
                Journal
                PHARH2
                Pharmaceuticals
                Pharmaceuticals
                1424-8247
                January 2024
                January 09 2024
                : 17
                : 1
                : 85
                Article
                10.3390/ph17010085
                ba06e87b-9087-4d32-8952-e854dd45b662
                © 2024

                https://creativecommons.org/licenses/by/4.0/

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