The Aetiological Causes Of Schizophrenia

For the past fifty years treatment of schizophrenia has been marked by its basis on the dopamine hypothesis for schizophrenia. However, this model for the disease and its subsequent treatment have left many patients without relief or help in dealing with this disease which has lead to a search for a better model. The dopamine model lacks the recognition of a whole range of symptoms associated with the disease and therefore can not be an accurate basis for treatment. More recently, there has been a shift to the glutamate hypothesis which has been shown to more accurately characterize the wide range of symptoms experienced by patients living with this disorder as well as the possibility in improvements for drug treatments.

Dopamine is a neurotransmitter known to be involved in regulating mood and behaviour, amongst other things. Schizophrenia is associated with an overactivity of dopamine in the brain, and this may be associated with the delusions and hallucinations that are a feature of this disease.

A third example of a neurological cause of schizophrenia is what is known as the dopamine hypothesis. This hypothesis is the idea that irregular levels of dopamine, in the case of schizophrenia, high levels of dopamine, are linked to some of the symptoms of schizophrenia (Eagleman & Downer, 539). This idea was thought of because of the findings on the use of amphetamines causing a rise in dopamine in the brain as well as the rise of the symptoms of schizophrenia (Seeman & Lee, 1975)( Eagleman & Downer, 538).

An excess in dopaminergic, and a deficit in glutaminergic (specifically NMDA) signalling correspond to positive and negative symptoms respectively. The NMDA antagonist MK-801 is used in animal models of schizophrenia, while paranoid and persecutory delusions are typical of methamphetamine users. In those with an

Schizophrenic patients are thought to have higher dopamine levels in their brains (overactive dopamine system). Many antipsychotics are designed to block dopamine receptors, and bind them, helping patients to improve and experience less severe symptoms, further proving the dopamine hypothesis. It was also found that drugs that increase dopamine levels (amphetamines) have caused more psychotics symptoms. This could partially result in a few psychotic symptoms occurring in the illness (GROMISCH, 2013).

Schizophrenia is universally considered to function on a neurological level, with various studies claiming that several different types of neurotransmitters are thought to contribute to the manifestation of schizophrenia in the brain (Carlton, 1984). These findings have encouraged the development of various hypotheses for the cause of schizophrenia, one of these includes the dopamine theory (Carlton, 1984). The theory originated out of research on the dopamine-blocking actions of initial antipsychotic drugs (Moncrieff, 2009). Pharmacological studies researching the use of drugs to treat schizophrenia found that, drugs which decrease dopaminergic activity in the brain such as, Clozapine and Haloperidol, are considered to be antipsychotics, whilst

There are primary neurological brain abnormalities in individuals with schizophrenia. According to Fusar-Poli (2009), schizophrenia is delineated by prefrontal activity and elevated striatal dopaminergic functions. These elevations in striatal dopamine activity and prefrontal cortical dysfunctions (Fusar-Poli, 2009). Along with other abnormalities in white matter as well as, having been observed in the right superior frontal gyrus, left middle frontal gyrus, bilateral parahippocampal gyrus, adjacent to the right caudate head, right thalamus, left insula, left lentiform nucleus, left fusiform gyrus, and bilateral claustrum (Antonius, 2011). The study of these findings may assist us to understand their role in the severity of the schizophrenia disorder symptoms (Antonius, 2011).

Schizophrenia has been associated with the dysregulation of many neurotransmitter systems. Large amounts dopamine is the oldest and most widely accepted theory of the pathophysiology of schizophrenia and stems from identification of dopamine D2 receptor blockade as the mechanism of action of antipsychotics. Dopamine D2 binding sites are increased in a person with schizophrenia, which contributes to cognitive impairment. The modern day understanding is suggested that a hyperactive mesolimbic and a hypoactive mesocortical dopamine system underlie the 'positive ' and 'negative ' symptoms that are seen in schizophrenia. Serotonin, glutamate, GABA and acetylcholine dysregulation have also been implicated in the pathogenesis of schizophrenia, in addition to dopamine. Glutamatergic signaling is attenuated in schizophrenia and is distinguished by a loss of NMDA receptor-mediated excitatory neurotransmission. GABA levels are also attenuated due to down regulation of GABA transporter (GAT) gene expression. “There is a concordant up regulation of GABAA receptors, which may contribute to the alterations in neural synchrony and consequently working memory impairment” (tocris.com, 2015).

Schizophrenia is a chronic neurological disease that results in a combination of positive, negative, and cognitive symptoms. Positive symptoms of Schizophrenia include hallucinations and delusions. Negative symptoms of Schizophrenia most commonly consist of avolition, anhedonia, and alogia. Cognitive symptoms affect the person’s cognition. Patients with the disorder have disorganized speech and behavior, deficits in learning and memory, as well as deficiencies in abstract thinking and problem solving. Positive symptoms of Schizophrenia are commonly attributed to the abnormally high levels of dopamine (Konradsson-Geuken, slide 25). While there is no current cure for Schizophrenia there are different treatments that prove to help certain aspects of the disorder.

Schizophrenia is a multifaceted disorder, where an extensive list of contributing factors have been revealed. Schizophrenia, as a mental illness, can be defined as a chronic, debilitating brain disorder which results in reality distortion and disrupted thoughts. Such an illness is then further subcategorised, where specifically withdrawal from the environment (behavioural aspect), and a noticeable deterioration in daily functioning (cognitive aspect) can be observed. In order to fathom the aetiological factors behind schizophrenia disorder, much research has been conducted. However, such research has revealed concerns for past theories attempting to explain the aetiology of schizophrenia. It is argued that a given theory may explain the cognitive

The dopamine hypothesis of schizophrenia as highlighted by Stone et al 2007 is seen as the principal explanatory model of antipsychotic drug action. The formulation of dopamine hypothesis was partly based on neuro pharmacological research that centred

To further compare the dopamine hypothesis, the Neurological substrates including errors in neurotransmitter levels. Some studies have suggested that negative, disorganized, and some positive symptoms may possibly could result from damage occurring to the neural system itself (Basso et al. 1998). The most frequently found findings in brain scans of those diagnosed with schizophrenia have included enlarged cerebral ventricles and reduced cortical volume especially in the temporal and frontal lobes in comparison to scans from non-schizophrenics. Post-mortem examinations have revealed a reduction of neuron density and size in the limbic, temporal and frontal regions of the brain and the connections between the neurons are noticeably disorganized.

Schizophrenia is a type of brain disorder that has been the center of attention in the past decade. Schizophrenia is such a complex disorder, its exact pathophysiology is unknown. Studies illustrated that neural circuits, functional deficits and the dysregulation of multiple pathways on different points of the brain all contribute to the pathophysiology of this disorder [1]. Strong evidence suggests the interaction of dopaminergic, GABAergic, glutamatergic, and cholinergic neurotransmitter systems play a role in the pathophysiology of this disorder [2]. For several decades, Involvement of dopamine neurotransmitter (DA), has dominated schizophrenia theories. However, it can’t explain the biological bases needed

It is involved with a person’s movement, thoughts, wellbeing as well as their feelings of pleasure (Veaugue, 2007).According to the dopamine hypothesis, when high levels of dopamine are found in the mesolimbic and when low levels of dopamine found in the prefrontal cortex, symptoms of schizophrenia will occur. When the cortical pathway through the nucleus accumbens is disturbed, there will be an increase subcortical release of dopamine, which in turn causes the D2 receptor to be activated. This process will result in positive symptoms of schizophrenia forming. The reduction of the D1 receptor found in the prefrontal cortex together with the decrease of activity in the nucleus caudatus will cause negative symptoms of schizophrenia (dopamine). The dopamine hypothesis is the most accepted hypothesis, yet scientists are still unsure of why there is an excess of dopamine in the body (article 1?).Glutamate is another neurotransmitter that could possibly be a causing factor in schizophrenia. Glutamate helps with learning as well as the encoding of memory. A schizophrenic person will have a lower amount of Glutamate in their body. Dopamine as well as Halucinatnic drugs-PCP- block the glutamate receptor sites, lowering the amount of Glutamate in the body (Veague, 2007).Acetylcholine function is participates in the movement, automatic function learning and memory in the brain. Therefore when acetylcholine is deficient it will cause the persons memory and learning ability to be affected, this is a schizophrenic symptom (book).Serotonin’s function is controlling mood, appetite and sleep. If there the level of serotonin has decreased (as in schizophrenia) then it will lead to the symptoms of depression as well as anxiety (book).GABA plays a vital role in the central nervous system and it take part in moods. In schizophrenia the level is reduced therefore it causes the symptoms of anxiety

Schizophrenia is a severe mental disorder affecting about 1% of the population worldwide. Although the dopamine (DA) hypothesis is still keeping a dominant position in schizophrenia research, new advances have been emerging in recent years, which suggest the implication of white matter abnormalities in schizophrenia. In this paper, we will briefly review some of recent human studies showing white matter abnormalities in schizophrenic brains and altered