DAYAODAO, JENELETH S.

BSN3A

3-24-15

SCHIZOPHRENIA

Scientists think interactions between genes and the environment are necessary for
schizophrenia to develop. Despite epidemiological evidence showing different rates of
schizophrenia in sociocultural groups that would be considered genetically similar, the causal
role of the environment is still hotly contested.
According to Vereczkei A. et al. (2011), Schizophrenia is a complex, devastating brain
disorder with clear genetic and environmental contributions to the emergence of the disease. In
the last several decades of research hundreds of millions of dollars were spent of the elusive
search for schizophrenia susceptibility genes, but the results have been meager. Researchers have
identified a number of genetic variants that predispose the brain to developing the disease, yet
alone they can explain only a very small number of the schizophrenia occurrence. Vulnerability
in DISC1, NRG1, DTNBP1, RGS4, KCNH2, COMT, AKT1 and other putative schizophrenia
genes, together with copy number variants, leave unexplained the vast majority of diseased
cases.
Os et al. (2003) cited that a familial vulnerability to schizophrenia is agreed even though the
exact genes involved seem elusive.
Scientists believe several genes are associated with an increased risk of schizophrenia,
but that no gene causes the disease by itself. In fact, recent research has found that people with
schizophrenia tend to have higher rates of rare genetic mutations. These genetic differences
involve hundreds of different genes and probably disrupt brain development. The illness occurs
in 1 percent of the general population, but it occurs in 10 percent of people who have a firstdegree relative with the disorder, such as a parent, brother, or sister. People who have seconddegree relatives (aunts, uncles, grandparents, or cousins) with the disease also develop
schizophrenia more often than the general population. The risk is highest for an identical twin of
a person with schizophrenia. He or she has a 40 to 65 percent chance of developing the disorder.
Scientists found small changes in the distribution or characteristics of brain cells that likely
occurred before birth. Some experts think problems during brain development before birth may
lead to faulty connections. The problem may not show up in a person until puberty. The brain
undergoes major changes during puberty, and these changes could trigger psychotic symptoms.
Scientists have learned a lot about schizophrenia, but more research is needed to help explain
how it develops.

The brains of people with schizophrenia look different than those of healthy people. For
example, fluid-filled cavities at the center of the brain, called ventricles, are larger in some
people with schizophrenia. The brains of people with the illness also tend to have less gray
matter, and some areas of the brain may have less or more activity.
Studies of brain tissue after death also have revealed differences in the brains of people with
schizophrenia.
Scientists consider that an imbalance in the complex, interrelated chemical reactions of the
brain involving the neurotransmitters dopamine and glutamate, and possibly others, plays a role
in schizophrenia. Neurotransmitters are substances that allow brain cells to communicate with
each other. Scientists are learning more about brain chemistry and its link to schizophrenia.
The study of Lawrence Kegeles mentioned that in patients with schizophrenia, cognitive
problems and negative symptoms are caused by too much or too little dopamine in certain brain
regions. Since postmortem studies reveal that dopamine cells are not damaged, the Columbia
researchers hypothesize that schizophrenia may be caused by poor dopamine regulation in
certain parts of the brain.
Many environmental factors may be involved, such as exposure to viruses or malnutrition
before birth, problems during birth, heavy adolescent marijuana use, and other not yet known
psychosocial factors. Social scientists and clinicians are convinced that social factors cause
schizophrenia and, therefore, that behavioural or environmental change might offer a more
tangible route to prevention than gene manipulation. Few would contest the fact that mental
states are influenced by the individual's social environment. Follow-up research has
demonstrated that the post-onset course of ICD, DSM and RDC psychotic disorders is extremely
sensitive to variation in the social environment. It is logical to assume that the same social
environment could play a causal role in the onset of psychotic mental states. This assumption is
now supported by evidence.

REFERENCES:
Retrieved March 20, 2015, from
http://www.annualreviews.org/doi/abs/10.1146/annurev.psych.55.090902.141950?
journalCode=psych
Retrieved March 20, 2015, from http://www.ncbi.nlm.nih.gov/pubmed/22239579
Retrieved March 20, 2015, from http://bjp.rcpsych.org/content/182/4/291