A Summary of the Specific Theory about the Possible Causes of Schizophrenia
The exact causes of Schizophrenia are not known. However, researchers have come up with theories that try to explain them. Many researchers, including Yuan et al. (2017) believe that a combination of genetic factors, brain chemistry, brain structure, and environmental factors leads to the development of the disease. In the genetic etiology of schizophrenia, copy number variants (CNVs) is implicated strongly (Marshall et al., 2017). The problem is that genome-wide investigations of the role of CNVs in the development of the disease require large samples, which may not be readily available. Additionally, the general role of genome structure in causing schizophrenia and other mental illnesses is still developing (Marshall et al., 2017). Scientists believe that CNVs can cause neurological problems because they have polygenic effects and can alter gene dosage. Also, CNV deletions are more likely than CNV duplications to cause Schizophrenia because they result in the loss of function associated with the deleted gene (Yuan. Et al., 2017). Large CNVs also have more consequences than smaller CNVs because they affect more genes and regulatory regions.

You're lucky! Use promo "samples20"
and get a custom paper on
"Schizophrenia: Review of Research"
with 20% discount!
Order Now

A Summary of the Purpose and Method of the Published Study of Step 2
The purpose of the published study I chose in step 2 is to identify original CNVs that increase the risk for schizophrenia among individuals. The study attempted to accomplish this purpose by using two groups of samples also called discovery cohorts. Both groups were ethnically homogeneous to increase the likelihood of success. The researchers also attempted to achieve the purpose by replication of results in large, meaningful, and representative samples. The method used by the researchers was microarray data association. The researchers collected DNA samples from 12,398 individuals from different parts of the world. The researchers also used a control sample of 17,945 individuals. The control group served an important role for purposes of comparison and the establishment of disparities if they exist between them and the experimental sample. The researchers collected the data from nine centers from around the world. The published study needed to use a large sample because doing so is the surest way of replicating the results.

A Summary of the Results and Conclusions of the Published Study of Step 2
The study implicated one original locus in the development of schizophrenia. The main outcome measured by the researchers was the statistical increase in the rate of specific CNVs in the experimental sample versus the control group. The results showed that gene removal within the 16p11.2 localities can lead to the development of a disease. The researchers found deletion in the 16p11.2 loci in 13 out of 13 850 cases. Deletion in this locus also occurred in 3 of 19 954 members of the control population. Based on these results, the researchers concluded that deletions at distal 16p11.2 increase the chances of developing schizophrenia and similar diseases. There are nine genes in the distal 16p11.2 localities. Several genes here have been shown to play a role in the advancement of neurological diseases. Some of these genes have also contributed to glucose homeostasis and body weight regulation. The researchers also observed that the gene deletion extended to other areas of the telomere in approximately half of the experimental sample. The researchers did not observe such extension in the control population. Hence, the researchers identified 8 additional genes where deletion can occur leading to schizophrenia.

Personal Analysis of the Study
the study provides important findings that add to the world’s understanding of the causes of schizophrenia. The findings also provide an additional locus to the CVNs that increase the chances of developing schizophrenia. The study has its strengths in that it uses a sufficiently large sample size and a control population. The main weakness of the study is the type of data collected and the analysis of the same. In the study, the researchers were only looking for the statistical increase in the rate of specific CNVs in the sample and the control population. Increases in CVNs may not clarify a hypothesis.

A Summary of the Current State of Our Knowledge Regarding the Causes of Schizophrenia
after reviewing various research articles, I am convinced that CVNs have a role in the development of schizophrenia and other neurological diseases. Most researchers are convinced that CVNs have a role in the development of schizophrenia because numerous studies have shown the existence of a correlation between the two. The only thing that lacks at the moment is an explanation of how CVNs actually cause schizophrenia. Knowledge about the development of the disease is scanty, and people are uncertain. Thus, there is a need for more research in this area to produce new reliable information that can influence the creation and utilization of preventive measures.

How I Might Design a New Study and what the Purpose Would Be
Understandably, no study can provide all the answers to an existing problem. In fact, studies build on each other and form an intricate web of connectedness. Based on the design and findings of this study, I might create a new research whose purpose would be to probe CVNs and why and how they multiply. The research will go into details about the characteristics of CVNs, and why some are large while others are smaller. Having an in-depth understanding of the specific characteristics of the CVNs is essential to the understanding of its impact on the development of schizophrenia and other neurological conditions. The understanding will also help the scientific scholarship create treatment regimens that focus on the elimination of causative elements as opposed to managing symptoms.