Similarities And Differences In Biological Mechanisms Between Schizophrenia And Depression University Of Hertfordshire Essay

3349 words - 14 pages

PSY3 Brain Disorders 14141847
Discuss the evidence that while depression and schizophrenia are distinct psychiatric disorders, there may be some parallels and/or similarities as well as differences in the underlying biological mechanisms. Refer in your answer to recent experimental studies that have advanced our understanding of the underlying causes and the brain pathology of these two disorders.
Schizophrenia is a disorder categorised by a separation between thought and reality. It involves positive symptoms such as hallucinations and delusions as well as negative symptoms such as anhedonia. Depression or ‘affective disorders’ consists of major depressive disorder and bipolar disorder. Both involve a low mood and lack of motivation across numerous aspects of day-to-day life with bipolar also including episodes of mania. These disorders at face value sound incredibly different from one another due to having many distinguishable features. Overall, depression and schizophrenia are two long-term brain disorders with a distinct criterion which is used for diagnosis. However, some may argue that the features of these two illnesses can overlap in certain areas. The underlying biological mechanisms of both schizophrenia and depression have various similarities and differences which this essay will explore.
Eugen Bleuler (1911/1950) invented the term schizophrenia, which translates to ‘split mind’, meaning a break from reality. Prevalence is approximately 1% across all sexes and cultures developing around late adolescence to young adulthood onwards (Mueser & McGurk, 2004). Cognitive, positive and negative symptoms but be present for the diagnosis of schizophrenia. Positive symptoms are well-known in relation to schizophrenia as they are the symptoms which present themselves openly, they include thought disorder (disorganised, irrational thinking), hallucinations (sensory experiences which contrast to reality) and delusions (beliefs which contrast to reality). Cognitive and negative symptoms tend to overlap with one another, with negative symptoms including a dampened emotional response and lack of initiative and cognitive symptoms including lack of attention and low psychomotor speed.
Major depressive disorder is a type of affective disorder which can range in severity. Although many people feel depressed occasionally, diagnosis of depression occurs when this low mood extends over a long period of time and cannot be justified by reality (e.g. bereavement). It has a prevalence of 3% in men and 7% in women which implies that it is the fourth leading cause of disability (Kessler et al., 2003) and can occur at any point in an individual’s life. Other than a low mood, people characterised depression by a lack of energy and slow speech as well as lack of pleasure (i.e. anhedonia). Sleep is also an important factor in relation to depression, as circadian rhythms are disrupted, causing those with depression to oversleep or only have shallow sleep. Those with bipolar disorder also have these depressed episodes but alongside episodes of mania, which can include a sense of euphoria, nonstop motor activity and a sense of grandiosity. However, bipolar disorder has a much lower prevalence and the gender ratio is more evenly split.
Whilst these are clearly two distinct disorders, it is vital we shine light on the fact that both schizophrenia and depression have similar negative symptoms. The negative symptoms of depression include avolition, anhedonia and anergia. These negative symptoms are also seen in those with schizophrenia, indicating some form of parallel within the biological constructs to produce these behaviours. However, there are slight differences in the production of these symptoms. Bottlender et al. (2003) assessed the negative symptoms in schizophrenic, depressed and control groups with the Scale for the Assessment of Negative Symptoms (SANS). They found that whilst depression and schizophrenia groups had high SANS ratings, the negative symptoms in depression seemed to be a product of the depressive symptoms, whereas for those with schizophrenia, the negative symptoms were distinct from the positive symptoms. Additionally, Chuang et al. (2014) believes the pathophysiological components of the negative symptoms in schizophrenia and depression are different, with the negative symptoms for depression being associated with a high grey matter volume in the bilateral cerebellum and the negative symptoms in schizophrenia being associated with white matter volume in the left anterior limb. Therefore, whilst there are prominent parallels in negative symptoms between the two disorders, studies indicate they may stem from different biological mechanisms.
Abnormalities in brain structure among those with depression and schizophrenia in comparison to controls is also another similarity between the disorders, especially due to the fact many of the same regions are involved. However, each disorder has its own individual abnormalities separate from each other. Enlarged ventricles are frequently seen in schizophrenia. Gaser, Nenadic, Buchsbaum, Hazlett and Buchsbaum (2004) believe this is due to regional specific volume loss. 39 people with schizophrenia underwent magnetic resonance imaging (MRI) scans to find thalamic shrinkage and loss of various other brain tissue is a critical factor contributing to ventricular enlargement. Further evidence comes from Gutierrez-Galve et al. (2010) who discovered that patients with schizophrenia and their non-diagnosed relatives both show loss of grey matter in the frontal and temporal cortex, suggesting interplay between genetics and cortical development.
Many of the brain regions involved in depression also play a role in schizophrenia, suggesting there may be similar qualities. Regions including the medial prefrontal cortex (MPFC), hippocampus and ventromedial parts of the basal ganglia all have a role. Drevets, Price and Furey (2008) summarised structural abnormalities in depression, stating that the MPFC is part of a larger cortical network which includes structures such as the anterior temporal cortex, entorhinal cortex and parahippocampal cortex. Damage to the system can cause abnormal emotional behaviour and disturbances in visceral control, both of which are known to be symptoms of depression. This is supported by Mayberg et al. (2005) who tested frontal and subcortical regions in treatment-resistant depressed participants using deep brain stimulation (DBS). They found improvement in behaviour after DBS to the subgenual anterior cingulate cortex (ACC), which is in the frontal cortex. The frontal cortex plays a critical role in the development of depression and more specifically, the ACC is used as a focal point for emotion regulation and therefore used for antidepressant treatments.
Another parallel is present as the frontal cortex is well-known to be damaged in those with schizophrenia. Using functional MRI scans, Callicott et al. (2000) found that N-acetylaspartate concentrations in the dorsolateral prefrontal cortex were significantly lower in those with schizophrenia than controls which in turn affected working memory performance, displaying how this brain abnormality affects those with the disorder. This provides solid evidence that the frontal cortex plays an enormous role in both schizophrenia and depression, making the two disorders similar in several aspects such as handling emotions and visceral functions.
The anterior cingulate cortex (ACC) monitors cognition and emotion as well as connects the limbic system to the prefrontal cortex. It is affected in both schizophrenia and depression which therefore explains the parallels in the disorder in relation to emotion control. Mouchlianitis et al. (2015) investigated antipsychotic treatment resistance in a schizophrenic sample by studying glutamate levels in the ACC and found that glutamate levels were higher in treatment-resistant patients in comparison to treatment-responsive. This suggests the ACC is associated with treatment-resistant schizophrenia and therefore displays the parallel of the ACC in depression and schizophrenia. Additionally, the ACC also acts as an inhibitor for the amygdala which is another area damaged in both schizophrenia and depression. This affects the acquisition and expression of negative emotions in these disorders in different ways.
To further support that emotions are affected in schizophrenia and depression due to brain structures, studies focusing on the amygdala also provide evidence of their similarity. For example, the amygdala has a role in interpreting fear. Hall et al. (2008) found when schizophrenic and control participants looked at fearful faces versus neutral, those with schizophrenia had a decrease in amygdala activity to the prior in comparison to the latter, but this was due to a spike in activation to the neutral faces, indicating inappropriate activation of the amygdala in schizophrenia.
There is a parallel between this and the use of the amygdala in depression. Sheline et al. (2001) conducted functional magnetic resonance imaging (fMRI) to compare amygdala activation in depressed patients and control subjects whilst they responded to faces displaying emotions. They found that depressed participants tend to have overactive left amygdala activation, especially to fearful faces which is reduced after anti-depressant treatment, further highlighting the amygdala’s role in depression. Whilst there are similarities between schizophrenia and depression as they both have deficits in the amygdala, it can be argued that the deficit is entirely different, as those with schizophrenia have an underactive amygdala and those with depression have an overactive one.
Neural mechanisms within brain structures are responsible for the deficits in both schizophrenia and depression. For schizophrenia, overactive dopaminergic synapses are a key factor in the development of the disorder as dopamine is an inhibitory neurotransmitter which plays a role in reward-motivated behaviour. The revised dopamine hypothesis suggests that the imbalance of dopamine causes an increase of positive symptoms of schizophrenia. Laruelle et al. (1996) injected amphetamine, which is known to stimulate the release of dopamine into both schizophrenic and control participants and found that there was a release of more dopamine in the striatum of participants with schizophrenia as well as an increase in positive symptoms. However, this hypothesis is one of the most endured in schizophrenia literature, and therefore has been revised many times. Others now argue abnormalities in acetylcholine and serotonin alterations are also involved in schizophrenia, providing a similarity between schizophrenia and depression.
Dopamine is of interest in bipolar disorder as well as schizophrenia. This is observed in Jauhar et al.’s (2017) study, who investigated dopamine and how it affects psychosis in both those with schizophrenia and bipolar. Using bipolar, schizophrenia and control participants, Jauhar and colleagues used positron emission tomographic scans to investigate the dopamine synthesis capacities and found elevated dopamine synthesis capacity in both those with bipolar and schizophrenia. The similar display of dopamine in these two disorders explains the parallel psychotic symptoms.
The main neurotransmitters for depression seem to be monoamines such as serotonin and norepinephrine. The monoamine hypothesis suggests that depression is caused by insufficient activity of monoaminergic neurons. Rationale stems from monoamine agonists helping to reduce the symptoms of the disorder whereas monoamine antagonists such as reserpine can produce depressive symptoms (Carlson & Birkett, 2017). A well-known procedure which supports the role of serotonin in depression is the tryptophan depletion procedure (Delgado et al., 1990) which involves giving patients with depression who were currently well a low tryptophan diet followed by an amino acid ‘cocktail’ which contained no tryptophan. Tryptophan is the precursor of serotonin therefore the uptake of these amino acids without tryptophan caused low levels of it in the brain, in turn lowering serotonin. This caused many of the patients to relapse back into depression but quickly recover once returning to a normal diet. This study has been replicated and strongly supports the vital role of serotonin in depression.
Whilst serotonin is much more focal in depression, more studies are beginning to surface suggesting that serotonin and 5HT transporters play a role in schizophrenia also. Some studies suggest serotonin contributes towards the negative symptoms of schizophrenia and that serotonin antagonists have an antipsychotic effect on these symptoms due to serotonin synaptic receptors being hyperactive (Bleich, Brown, Kahn & van Praag, 1988). Therefore, many atypical antipsychotic drugs such as clozapine work by blocking serotonin receptors to stimulate the monoamine or at least reduce dopamine levels whereas typical antipsychotic drugs solely focus on dopamine receptors (Meltzer & Massey, 2011). Atypical antipsychotic treatment produces an abundance of evidence displaying its effectiveness therefore, in turn, it shows the role of serotonin and its link to schizophrenia. With these studies in mind, a clear similarity is shown between serotonin and its influence on both schizophrenia and depression.
Although the cause of schizophrenia has not been completely determined, people favour the concept of a genetic predisposition otherwise known as a ‘schizophrenia susceptibility’ gene. Heritability is high for schizophrenia which is displayed through an abundance of evidence. Twin and adoption studies is an example of this evidence as these participants may share the ‘schizophrenia susceptibility’ gene. For example, Gottesman and Bertelsen (1989) examined the rate of schizophrenia in children of discordant monozygotic twins and discovered that the percentage of these children who developed schizophrenia was strikingly similar. The children whose parents did have schizophrenia was 16.8% whereas the children who did not was 17.4%. Paternal age also suggests a heritable biological basis for schizophrenia. Several studies have indicated that the older the father of the child is, the more likely the onset of schizophrenia due to mutation during spermatogenesis. Perrin, Brown and Malaspina (2007) hypothesise that the ‘dysregulation of epigenetic processes’ could link paternal age and schizophrenia. Epigenetics cause heritable changes in gene expression therefore mutations can cause issues for those who inherited them. Paternal age acts as a marker of epigenetic errors can occur in somatic cells causing an increased susceptibility to schizophrenia. However, this finding is still in its early days, and therefore much more research must be done to reach a conclusive answer.
Developing an affective disorder such as major depressive disorder or bipolar is also heritable, meaning there is some form of genetic predisposition. Guffanti et al. (2016) studied lifetime rates of major depressive disorder in 65 multi-generational families over a 30-year period and found that the heritability in this high-risk sample was 67% indicating a heritable genetic component in depression. Additionally, it is well-known that circadian rhythms play an important role in the development of affective disorders. McGrath et al. (2009) discovered RORB, a circadian rhythm gene, was associated with the paediatric bipolar phenotype, indicating its importance in children with bipolar, this however, is still open to ongoing study.
Looking at the given evidence, a parallel can be suggested between depression and schizophrenia due to its heritable components. If both require a genetic disposition and are possibly polygenic, then some genes may overlap, especially since comorbidity rates for schizophrenia are high. Additionally, when taking antidepressants concurrently with anti-psychotic medication, beneficial effects can occur (Bosanac & Castle, 2012).
One large difference between schizophrenia and depression is the imbalanced amount of evidence for environmental influences of each disorder. For schizophrenia, the ‘susceptibility gene’ can be triggered by an environmental influence, but there is lacking evidence for environmental causes for depression. Epidemiology studies confirm various prenatal and postnatal environmental causes, such as the seasonality effect, which states that a person born in the late winter or early spring has a higher chance of developing schizophrenia. Other postnatal environmental effects include population density. Pedersen and Mortensen (2001) discovered that the longer a person lives in the city, the more likely it becomes that person will develop schizophrenia. This would be considered a difference between schizophrenia and depression, as schizophrenia has a much higher environmental risk.
Overall, it can be concluded that whilst biologically, there are plenty of overlaps between schizophrenia and depression which present us with various parallels, no two comparisons are exact. This is mirrored well in what we see of each disorder, as both may have issues with emotion or pleasure due to similarly abnormal structures and neurotransmitters, but these issues are not identical. Compiling this evidence and cleared any confusion as to why these two disorders are diagnosed completely separately, despite depressive symptoms creeping over into the schizophrenia criterion.
References:
Bleich, A., Brown, S. L., Kahn, R., & van Praag, H. M. (1988). The role of serotonin in schizophrenia. Schizophrenia Bulletin, 14(2), 297-315.
Castle, D., & Bosanac, P. (2012). Depression and schizophrenia. Advances in psychiatric treatment, 18(4), 280-288.
*Bottlender, R., Sato, T., Groll, C., Jäger, M., Kunze, I., & Möller, H. J. (2003). Negative symptoms in depressed and schizophrenic patients: how do they differ? The Journal of clinical psychiatry, 64(8), 954-958.
Callicott, J. H., Bertolino, A., Mattay, V. S., Langheim, F. J., Duyn, J., Coppola, R., & Weinberger, D. R. (2000). Physiological dysfunction of the dorsolateral prefrontal cortex in schizophrenia revisited. Cerebral cortex, 10(11), 1078-1092.
*Carlson, N. R., & Birkett, M. A. (2017). Physiology of Behaviour. Essex: Pearson Education Limited.
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*Hall, J., Whalley, H. C., McKirdy, J. W., Romaniuk, L., McGonigle, D., McIntosh, A. M., ... & Sprengelmeyer, R. (2008). Overactivation of fear systems to neutral faces in schizophrenia. Biological psychiatry, 64(1), 70-73.
Hall, J., Trent, S., Thomas, K. L., O’Donovan, M. C., & Owen, M. J. (2015). Genetic risk for schizophrenia: convergence on synaptic pathways involved in plasticity. Biological psychiatry, 77(1), 52-58.
*Jauhar, S., Nour, M. M., Veronese, M., Rogdaki, M., Bonoldi, I., Azis, M., ... & Howes, O. D. (2017). A test of the transdiagnostic dopamine hypothesis of psychosis using positron emission tomographic imaging in bipolar affective disorder and schizophrenia. JAMA psychiatry.
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*Sheline, Y. I., Barch, D. M., Donnelly, J. M., Ollinger, J. M., Snyder, A. Z., & Mintun, M. A. (2001). Increased amygdala response to masked emotional faces in depressed subjects resolves with antidepressant treatment: an fMRI study. Biological psychiatry, 50(9), 651-658.

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