Anomalies in the Brain of a Schizophrenic

Anomalies in the Brain of a Schizophrenic By Isabella

Throughout the years, many misconceptions about schizophrenia have been formed. Abuse of MDMA and cannabis as well as “early neurodevelopmental” lesions were early theories as to the cause of schizophrenia. However, the coupling of new technologies and further study disprove these theories, yet several unknowns are still prevalent. Hopefully, new machine learning techniques and the advent of connectomics can reveal further insight into the undiscovered realm of schizophrenia.

The early signs and symptoms of schizophrenia make it a frightening disease. With typical onset in late adolescence to early childhood, early onset between the ages of 8 and 10, and late onset at the age of 45 and on, schizophrenia can strike at virtually any time. The plethora of effects—disorganized speech, absurd or suspicious ideas or beliefs, delusions ranging from persecution to grandeur—follow, altering the perception of the world to the schizophrenic. There are three main types of schizophrenia: paranoid, disorganized, and catatonic. Paranoid schizophrenics tend to have delusions of persecutions or grandeur, believing absurd and suspicious ideas, which consistently revolve around a central story. Their long term prognosis is better, as the symptoms appear later and they tend to function better. Disorganized schizophrenics’ symptoms appear gradually, rather than abruptly. They retreat into their fantasies and are characterized by disorganized thought, speech and an inability to bathe and feed themselves. Catatonic schizophrenics have issues with movement: they can rapidly shift from being in a stupor to being very excited, and often mimic others and automatically obey commands. Clearly, schizophrenia is an extremely debilitating disease and requires much more research, as there is no cure.

“To find the cause of schizophrenia, we must find some brain anomaly that is constant,” says Sebastian Seung. Throughout the years, modern science has discovered a few consistencies in the brains of schizophrenics. Researchers at Johns-Hopkins University have studied glia cells and their effect on cognition, as they believe that glia cell abnormalities—specifically astrocyte abnormalities—are just as important as neuronal abnormalities. They planted DISC 1 (Disrupted in Schizophrenia 1) gene mutations in mice and studied the effects. Astrocytes secrete the neurotransmitter D-Serine, which promotes glutamine transmission, believed to contribute to cognitive function; D-Serine is decreased in schizophrenics because DISC 1 metabolizes D-Serine faster, decreasing its prevalence. The mice bred with the mutant DISC1 protein in astrocytes did, as predicted experience decreased levels of D-Serine and consequently, schizophrenic-like symptoms. Further studies show a relationship between the disarray of pyramidal cells in the hippocampus and the severity of behavioral impairment associated with schizophrenia. Other studies show, through “interhemispheral crosstalk” that right handed people feel the effects of cannabis combined with schizophrenia more than left handed people. This may be an effect of another study regarding structural changes in the brain in relation to schizophrenia. These changes (whether they caused or are a result of schizophrenia is unknown) show ventricular enlargement in the posterior and temporal horn of the lateral cerebral vesicle, highly selective to the left hemisphere. The ventricular enlargements aren’t accompanied by an increase in glial cells. Another study suggests that developmental abnormalities related to schizophrenia are due to a faulty assembly of MAPs (microtubule associated proteins) because a deficiency in trophic cell receptors while another study notes an “increased prevalence of cavum septum pellucidum” in schizophrenics. While all these studies are major discoveries for furthering the understanding of schizophrenia, so many of these articles state that their evidence can point only to correlation; it isn’t known if the ventricular enlargements were present before schizophrenia struck or if they were there as a result of the schizophrenia. Many limitations inhibit these studies. As Sebastian Seung explains in his book, “Why are we still trying to use phrenology to explain mental differences? It’s not because the strategy is good. It’s because we have failed to come up with a better one…We know that size reveals little about function, but we look at it anyway because that’s what we can see with existing technologies.”

Again, the current studies of schizophrenia do lead to many developments in its treatment. But to gain a deeper understanding of this disease, more advanced technology is necessary. Hopefully, with machine learning, image segmentation and the new field of Connectomics, further advances in understanding neurological disorders can be achieved; we will go beyond the point of identifying correlations and understand, neuron by neuron and synapse by synapse how the brain malfunctions and how we can fix it.

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