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Traumatic brain injury: Schizophrenia Essay

Schizophrenia is a chronic mental disorder that affects approximately one percent of the population. Typically, the age of onset lies between the ages of 16 and 25, although in rare cases the symptoms start showing at a much younger age. The symptoms are separated into two distinct categories: negative and positive. Negative symptoms are normal, healthy behaviours that have been lost due to the disorder: in other words, they are a lack of function. Examples of negative symptoms include impaired attention and arousal (Nakumara, 2003), social withdrawal, and apathy. On the other hand, positive symptoms are behaviours that aren’t normally found in healthy individuals. These include delusions (David Kimhy, 2005), hallucinations of different modalities, and paranoia.

Traumatic brain injury (TBI) is nondegenerative damage to the brain that is caused by an environmental force. There are four types of TBI: concussion, contusion, anoxic, and penetrating injury. Many studies suggest that individuals suffering from (contusion?) TBI are at greater risk of schizophrenia than healthy individuals. Explain the types?

Recent research involving brain imaging technologies, correlational studies and animal experiments suggest there is a relationship between traumatic (?) TBI and schizophrenia.

Currently, treatment options for schizophrenia only aim to suppress its symptoms rather than dealing with the source of the problem itself. A known example of this is Chlorpromazine: the most widely used antipsychotic drug that blocks dopamine hormone receptors in brain cells. Since some positive symptoms of schizophrenia are caused by the overactivity of dopamine (Jauhar S, 2017), blocking the dopamine receptors will reduce the severity of these symptoms (Amrita Prakash Singam, 2011). However, a treatment that aims to reduce the overproduction of the hormone itself rather than blocking all dopamine receptors in the brain would be much more harmless and effective.

Development

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A study conducted by Flygt et al. (Journal of neuropathology & Experimental Neurology, 2016) aimed to

Glial cells are responsible for holding neuronal cells in place and providing them with protection, as well as maintaining homeostasis and myelination. Four major types of neuroglia can be identified in the central nervous system: Oligodendrocytes, Astrocytes, Ependymal cells and Microglia. Research by (Steve Goldman, 2017), (Hof PR, 2003), and (Dmitri Tkachev, 2003) suggests that dysfunctional glial cells are a biological cause of schizophrenic disorder. The reduced activity of macroglia in the central nervous system is thought to be the neurological cause of positive and negative symptoms seen in patients with schizophrenia.

Currently, treatment options for schizophrenia only aim to suppress its symptoms rather than dealing with the source of the problem itself. A known example of this is Chlorpromazine: the most widely used antipsychotic drug that blocks dopamine hormone receptors in brain cells. Since some positive symptoms of schizophrenia are caused by the overactivity of dopamine (Jauhar S, 2017), blocking the dopamine receptors will reduce the severity of these symptoms (Amrita Prakash Singam, 2011). However, a treatment that aims to reduce the overproduction of the hormone itself rather than blocking all dopamine receptors in the brain would be much more harmless and effective.

Recent research involving brain imaging technologies, correlational studies and animal experiments suggest there is a relationship between faulty neuroglia and schizophrenia.
This essay will focus on the genetic predisposition that triggers the symptoms seen in the disorder. More specifically, it will examine the extent to which the dysfunction of glial cells can be a neurological basis for schizophrenia. Research by (Steve Goldman, 2017), (Hof PR, 2003), and (Dmitri Tkachev, 2003) suggests that dysfunctional glial cells are a biological cause of schizophrenic disorder. On the other hand, research by (Devorah Segal, 2010) and (?) suggests that there is no correlation between the functionality of neuroglia and schizophrenic symptoms in affected individuals. This essay supports the first argument: The reduced activity of macroglia in the central nervous system is the neurological cause of positive and negative symptoms seen in patients with schizophrenia.

Goldman (2017) carried out a controlled animal experiment where researchers collected skin cells from patients with childhood-onset schizophrenia and created induced pluripotent stem cells: they are undifferentiated cells that through cell division can either divide into two stem cells or divide into any differentiated cell (one that isn’t a stem cell) found in the body. In this case, by controlling the extracellular environment they gave rise to glial progenitor cells (GPCs). These were then implanted into new-born mice’s brains, resulting in mice with human glial cells. There was also a control group of mice who were implanted with healthy human GPCs.

Researchers rapidly noted that the oligodendrocytes developed slower in mice with neuroglia taken from schizophrenic individuals. This led to insufficient myelination, and therefore the communication between neurons was limited, faulty and ineffective. In addition, researchers also observed a tardy development of astrocytes, which resulted in some neuronal synapses not having any protection or coverage.

The mice were then subjected to a series of behavioural tests. Results suggest that those injected with glial cells from individuals with schizophrenia were more prone to antisocial or anxious behaviour than those in the control group with healthy glial cells.

As the individuals whose skin cells were collected had childhood-onset schizophrenia, the cause of their disorder was most likely genetic factors rather than nurture. Since a cause-effect relationship between the activity of glial cells and manifestations of schizophrenia is established, Goldman’s study suggests that neuroglia (specifically, astrocytes and oligodendrocytes) which are genetically predisposed to be dysfunctional can cause childhood-onset schizophrenia.

However, there is a degree of uncertainty regarding the malfunction of the cells: it remains unclear whether it is caused by their defective genome or by the incompatibility of the human GPCs with the mice’s system. A simple way to deal with this obstacle would be to include a second control group of mice with their own biological glial cells, since this would provide with data to compare the mice with healthy human GPCs behaviour with.

(researcher bias with mice, expectancies, bright/slow rat- ask mr latham for that study)

(should I go into that much detail for a secondary study?)

Therefore, since (?) TBI is capable of damaging glial cells and considering that their malfunction can be a biological cause of schizophrenia, it makes sense that TBIs are often linked to the condition.

On the other side of the argument, Segal et al. (2010) conducted a (study or observation?) where a stereological nearest-neighbour estimator of spatial distribution -a method that estimates the distance between particles- was used to determine the density and distribution of oligodendrocytes in the anterior cingulate cortex (ACC) of “brains from 13 persons with schizophrenia and 13 controls matched for age”. Multiple studies have looked at abnormalities in the ACC as being a possible neurological basis for schizophrenia (Mark S. Todtenkopf, 2005) or (Alex Fornito, 2009).

The results showed that no significant differences in density or number of oligodendrocytes were found between the two controls. This suggests that oligodendrocyte distribution in the ACC isn’t abnormal in the brains of schizophrenic individuals.

Many studies suggest a relationship between anatomical dysfunctions of the anterior cingulate cortex and schizophrenic symptoms. The findings of Segal’s (observational study?) indicate that there might be a correlation, but that the schizophrenic symptoms are not due to the abnormal distribution of oligodendrocytes in that area. As discussed in Goldman’s study, introducing faulty human glial cells into mice’s brains is enough to arise negative symptoms of the disorder. This puts forward for consideration that anatomical dysfunctions of the ACC linked to schizophrenia may have an underlying cause and thus may arise as a consequence of it, but they might not be a direct neurological cause to the disorder.

Therefore, although this (observational study?) does suggest that there are no faulty support cells in the ACC of patients with schizophrenia, it is based on the assumption that a dysfunctional ACC is the cause of schizophrenia, which might not be the case.

Moreover, (something about a 27% difference of oligodendrocyte distribution in another brain area) (this basically backs up that oligodendrocyte dysfunction has a different location in the brain).

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