Schizophrenia Research Paper (original) (raw)
Related papers
Genetics and Schizophrenia: A Comprehensive Clinical Analysis
Srinivas Publications , 2022
Purpose: Genetics is a significant risk factor for schizophrenia. In the last decade, molecular genetics research has yielded groundbreaking results, fueling hope for uncovering the basic causes of schizophrenia. However, because of the complexity of the subject of study, it is nearly hard for nongeneticists (e.g., many physicians and researchers) to grasp and appreciate the genetic results and their limitations. This study tries to aid such comprehension by offering a brief summary of some of the most important methodologies and results in schizophrenia genetics, from its historical beginnings to its current state, as well as addressing some of the limits and issues that this field of research faces. In short, schizophrenia's genetic architecture has been shown to be very complex, diverse, and polygenic. Numerous common genetic variations with minor individual effects and uncommon, highly penetrant genetic variants with bigger effects make up the illness risk. Despite recent improvements in molecular genetics, we still have a limited understanding of the etiopathogenesis of schizophrenia and genotypeenvironment interactions. Our understanding of the molecular genetics of schizophrenia is quickly evolving thanks to genome-wide research. These research revealed rare copy number changes (mostly deletions) linked to schizophrenia, as well as frequent SNPs linked to schizophrenia alleles. But yet, it is necessary to combine all novel research findings with the existing results to get a more precise and comprehensive idea about genetics of schizophrenia. So the main purpose of this paper is to amalgamate the newest research findings with the existing information and spread this information in society to understand the biological roots of schizophrenia. Design/Methodology/Approach: Secondary data and information have been used to build the paper. All the information and new research findings have been taken from authentic journals/websites. Systematic clinical analysis has been done to create the paper more understandable to common population. More than fifteen articles have been systematically and thoroughly interpreted to derive the findings. Findings/Result: The findings suggest polygenic inheritance and genetic overlap between schizophrenia, autism, and bipolar illness. As further genetic discoveries are made, it is expected that the use of a variety of systems biology approaches will lead to the identification of molecular pathways implicated in the pathophysiologies of schizophrenia, as well as the development of new therapeutics. Originality and value: A novel approach has been taken to make the clinicians and people those who are in the field of providing care for schizophrenic patients to understand the genetic vulnerability of schizophrenia in a simplest and at most scientific way. The contents have been prepared and arranged such a way that even people those who are not belongs to the field, but interested to know more about schizophrenia and its genetic predispositions can make use of this article to enhance their knowledge.
Neuron, 2000
this syndrome is increased as well. Recently, chromo- † Departments of Psychiatry, Pharmacology, some 1q21-22 was identified as the location of a major and Radiology vulnerability locus for familial schizophrenia with suffi-University of North Carolina School of Medicine cient power to permit positional cloning of the underlying gene(s) (Brzustowicz et al., 2000). Environmental factors (including exposure to infectious, autoimmune, toxic, or traumatic insults and stress Introduction during gestation or childhood) also may play a role in Schizophrenia is a brain disorder that is expressed in the pathogenesis of schizophrenia, perhaps via subtle the form of abnormal mental functions and disturbed alterations of neurodevelopment (Marcelis et al., 1998). behavior. These manifestations characteristically ap-Moreoever, maturational processes including apoptopear in the late second and third decades of life as a sis, synaptic pruning, and myelination, occurring in the heterogeneous constellation of three classes of clinical postnatal period through adolescence, may unmask the features. Positive symptoms include delusions (false begenetic vulnerability to schizophrenia (Lewis, 1997; Jarliefs), hallucinations (false perceptions), and thought disskog et al., 2000; Raedler et al., 2000)
The Genetics of Schizophrenia: A Current, Genetic-epidemiologic Perspective
Schizophrenia Bulletin, 1993
In the "Special Report on Schizophrenia" published in the Schizophrenia Bulletin in 1987, the genetic basis of schizophrenia was reviewed. Here, we provide our perspective on the current status of this area of investigation, focusing largely but not exclusively on recent findings. Methodologically rigorous family studies have now clearly shown that schizophrenia substantially aggregates in families. Familial factors that predispose to schizophrenia also increase the risk for certain schizophreniarelated personality disorders and probably for some forms of nonschizophrenic nonaffective psychosis. Results from one new twin study and updates from two ongoing adoption studies continue to support the hypothesis that genetic factors play a major role in the etiology of schizophrenia. Little is known about how genetic liability to schizophrenia is transmitted, although statistical models suggest that transmission is probably not due solely to a single major gene. Schizophrenia is clearly a complex disorder in that gene carriers need not manifest the illness (incomplete penetrance), affected individuals need not have the gene (environmental forms or phenocopies), diagnostic uncertainties cannot be avoided, and different families may carry different susceptibility genes (genetic heterogeneity). Therefore, segregation or linkage analyses are far more difficult to perform with schizophrenia than with Mendelian genetic disorders. Given this complexity, it is not too surprising that no replicated positive evidence for linkage to schizophrenia has been reported to date. However, just as linkage analysis of schizophrenia should not be excessively embraced as the only form of viable genetic research in schizophrenia, it also shouldn't be prematurely spurned. If one or several genes of major effect exist for schizophrenia, large samples using new statistical and laboratory methodologies have a good chance of detecting them. The authors thus recommend a balanced research approach to the genetics of schizophrenia that includes traditional methods of family, twin, and adoption studies as well as a major effort in large-sample linkage studies.
Strength of the genetic effect in schizophrenia
The British Journal of Psychiatry, 1994
The Roscommon Family Study. I. Methods, diagnosis of probandsand riskof schizophrenia in relatives. Archives of General Psychiatry. 50, 527-540. Rsvsi.sy, A. M. & Rsvauty, M. A. (1987) The relationship of twinning to the familialâ€"sporadic distinction in schizophrenia.
Schizophrenia and the Question of Genetic Heterogeneity
Schizophrenia Bulletin, 1989
Despite major advances in psychiatric diagnosis during the past 20 years, boundaries of the schizophrenic syndrome remain elusive. Moreover, in pedigrees containing cases of schizophrenia there are marked between-pedigree differences with respect to prognosis, familial patterns of psychiatric illness, drug response, and especially association of affected status with a specific chromosomal locus. Such between-pedigree differences suggest the syndrome may be made up of several different diseases. Linkage of affected status to specific loci may aid in resolving genetic heterogeneity. Large multigenerational informative pedigrees may permit the separation into those that do and do not link to a genomic locus of interest. Admixture analysis of smaller informative pedigrees may permit separation of linked and unlinked pedigrees on the basis of differences in the recombination fraction. Finally, biological "markers" can be used before the genetic analysis to separate putative linked and unlinked pedigrees. The combined study of genetic linkage and clinical heterogeneity will aid in the resolution of etiological heterogeneity of schizophrenia and the delineation of meaningful diagnostic boundaries.
Comments on risk for schizophrenia
Schizophrenia research, 2005
Recent developments have significantly furthered understanding of genetic and environmental factors affecting risk for schizophrenia. Environmental effects, such as immigration, living in a city, and substance abuse have been found to be associated with later schizophrenia. Although the highest risk for schizophrenia is still having a monozygotic twin with schizophrenia (50%), the candidate genes claimed to be associated to date only yield a very small excess risk and all of these effects (environmental and genetics) increase the risk for schizophrenia by only 2-3 fold. Thus, given the low prevalence of the disorder in the general population (0.5-1%), they are not practical in predicting future illness. One possible strategy to make the currently known risk factors for schizophrenia more useful clinically is based on findings indicating that many of the genetic and environmental risks cited above are not specific for schizophrenia, but increase risk for psychopathology in general. A...