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The Pathophysiology Of Schizophrenia

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Schizophrenia is a unique disease in its pathophysiology. For their early lives, patients appear healthy. However, symptoms begin to appear during adolescence or early adulthood and may be triggered by changes in the brain during puberty. The first signs of the illness include anxiety, depression, changes in friends, sleep problems, irritability, dropping grades, and having trouble concentrating (Picchioni and Murray, 2007; National Institute of Mental Health (NIMH)). Delusions and hallucinations typically begin between the ages of 16 and 30 (NIMH).
One category of symptoms is referred to as positive symptoms. These include hallucinations involving any of the senses and attempting to make sense of these hallucinations often leads to delusions. …show more content…

Genetic mutations seen in people with schizophrenia may lead to abnormal brain development and neurotransmission. For example, mutations in NRG1, a gene located on chromosome 8, have been implicated in schizophrenia. This gene codes for a growth factor that is involved in neuronal development and differentiation as well as regulation of postsynaptic density. Additionally, DISC1, located on chromosome 1 at a balanced translocation breakpoint, is associated with schizophrenia. The protein coded for by DISC1 plays a role in both neuronal development and adult brain function through effects on the neurite architecture, migration of neurons, synaptic transmission, and intracellular transport. The DISC1 protein also interacts with phosphodiesterase 4B, resulting in the inactivation of cAMP, which has been reported to play a role in mood, memory and learning. Furthermore, RGS4, a gene located on chromosome 1, has been implicated in neuronal differentiation and studies have shown that brain tissue of schizophrenic patients show reduced expression of the RGS4 protein (DNA Learning Center). Scientists believe that the differences in neuronal distribution seen in schizophrenia patients occur prenatally and that these changes may result in the formation of impaired connections in the brain. In addition, imbalances in the …show more content…

These scientists identified 128 independent associations with schizophrenia encompassing 108 loci, 83 of which had not been previously reported. They found that among the loci that they identified, there was no evidence of non-additive or epistatic effects. 75% of the 108 loci identified in this study include genes that code for proteins and an additional 8% are located within 20kb of a gene. They found that there was an association with CACNA1C, CACNB2, and CACNA1I, which code for subunits of voltage gated calcium channels and have been suggested to play a role in other psychiatric disorders in addition to schizophrenia. Quantitative trait loci, those that regulate the expression of mRNA, were also implicated in conferring a risk for schizophrenia. There were also higher levels of expression of schizophrenia risk genes in tissues associated with immune function, which supports the hypothesis that immune dysregulation plays a role in schizophrenia. They also found that copy number variations that were linked to schizophrenia overlapped with those that are associated with autism spectrum disorder and other intellectual disabilities (Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014). However, some scientists hypothesize that genes alone are not sufficient for the development of schizophrenia

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