The Effects Of Myelin And Oligodendrocyte Dysfunctions

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

Expert’s reason that unevenness in the complicated interconnected chemical responses of the brain connecting the neurotransmitters dopamine and glutamate, and maybe others, performs a part in schizophrenia. Neurotransmitters are elements that permit brain cells to interconnect with each other. Experts are acquiring more about brain chemistry and its connection to schizophrenia. Similarly, in small methods the brains of people with schizophrenia appear diverse than those of healthful people. For instance, fluid-filled holes at the middle of the brain, called ventricles, are greater in certain people with schizophrenia. The brains of people with the disorder similarly manage to have less grey matter, and certain

Today, scientists at the University of Iowa are studying abroad how people suffering from the mental disorder, schizophrenia, may have less brain tissue than those who do not have the disorder. Schizophrenia deeply affects the brain and causes individuals to lose touch with reality and have unorganized thoughts, troubled perceptions and unsuitable emotions and actions. “Schizo” means split and “phrenia” means mind, however this does not mean that this is a split mind or personality disorder, like most people commonly mistake this as. In order to understand this disorder, we need to take a look at the actual condition and how it is defined, apart from other disorders, speculated causes, such as genes from

Genetics can cause differences in brain chemistry and biochemistry may be important in the development and maintenance of schizophrenia. The dopamine

Schizophrenia is a brain disease. Many studies have been conducted regarding the brain localization of schizophrenia. One study established that schizophrenia is characterized by significant loss in the grey matter of the brain. The loss was detected to be up to 25% in some areas and the damage was seen to begin at the parietal (outer) regions of the brain then spreading to the rest of the regions of the brain over a period of about five years ADDIN EN.CITE Rajagopalan1998923(Rajagopalan, MacBeth, & Varma, 1998)92392317Rajagopalan, MMacBeth, RVarma, SLXXY chromosome anomaly and schizophreniaAmerican Journal Medical GeneticsAmerican Journal Medical Genetics64-65811998( HYPERLINK l "_ENREF_9" o "Rajagopalan, 1998 #923" Rajagopalan, MacBeth, & Varma, 1998). Another study showed that patients who had the worst loss of brain tissue also exhibited the worst symptoms of schizophrenia such as hallucinations, psychotic and bizarre thoughts, hearing voices, depression and delusion ADDIN EN.CITE Conklin2002797(Conklin & Iacono, 2002)79779717Conklin, Heather M.Iacono, William G.Schizophrenia: A Neurodevelopmental PerspectiveCurrent Directions in Psychological ScienceCurrent Directions in Psychological Science33-371112002Sage Publications, Inc. on behalf of Association for Psychological Science09637214http://www.jstor.org/stable/20182759( HYPERLINK l "_ENREF_2" o "Conklin, 2002 #797" Conklin & Iacono, 2002).

Schizophrenia is a psychotic disorder characterized by distorted thinking, impaired emotional responses, poor interpersonal skills and a distortion of reality. It is the most common of psychotic disorders that, in most countries around the world, affects around 1 per cent of the population. In terms of explanations for the disorder, two central types of explanations arise – psychological explanations and biological explanations. Whereas psychological explanations tend to focus on cognitive, emotional and environmental factors that may cause the disorder, biological explanations tend to focus on genetic, biochemical and neuro-anatomical factors as the cause of the

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.

Schizophrenia is a complex and highly debilitating mental illness that we are currently unable to treat in any way that guarantees success or return to previous function. It affects around 1% of the population and is associated with a thirteen-fold increase in the likelihood of suicide, so its effective control is paramount (Gogos et al., 2015). There have been several hypotheses as to the cause of schizophrenia. Many link genetic and environmental factors, and dysregulations of neurotransmitters dopamine, glutamate, and serotonin (Egbujo, Sinclair, & Hahn, 2016). The dopamine hypothesis currently suggests that hyperactive dopamine transmission in the basal ganglia leads to psychosis and underactive dopamine transmission in the prefrontal

Over the last few decades Schizophrenia has become embedded in mainstream vernacular as any behavior or emotional response that is out of touch with reality. However even with its popularity heightened through movies and headline news stories, schizophrenia is still one of the most enigmatic and least understood disorders of the brain. With current research focused on the role of neurobiology and functioning on a cellular level, investigative analysis has merited new innovations towards its source, however a single organic cause for the disorder still eludes scientists. Although the foundation of the affliction is still unknown, its effects are well documented and over the next few pages will show the changes in the brain as the disease

The brain is composed of mostly grey and white matter. Grey matter contains most of the neuronal connections for the brain. It can be found on the outer surface of the cerebellum and around the spinal cord. “Observations have been made of reductions in the size and total neuron numbers, but not in neuronal density,” (Höistad, 2009, p. 3). This is an outstanding discovery when analyzing schizophrenia. White matter contains many neurons as well. Researchers pay close attention to these neurons and the myelination of the axons. “Interstitial white matter neurons have been found to be increased in prefrontal white matter and temporal white matter in subjects with schizophrenia, supporting further the presence of a neurodevelopmental abnormality in schizophrenia,” (Höistad, 2009, p. 3). This means that they white matter neurons never became myelinated and mature in parts of the brain. Problems like these can mess with the connections in the brain between neurons. Research like this highlight schizophrenia as being a developmental disorder of the brian, but more research is being done including other areas as well. “The pruning of axonal connections during brain development and maturation may be necessary for adequate formation of appropriate neuronal circuits,” (Höistad, 2009, p.

As we have seen, treatment of schizophrenia with antipsychotic drugs can have impressive results in terms of decreasing active symptoms, although it does nothing to alleviate negative symptoms or to improve cognitive functioning. Unfortunately, this kind of treatment has the drawback of extremely serious and even fatal side-effects. Newer generation atypical antipsychotics offer more hope, as they can treat both active and negative symptoms, and also improve cognitive functioning. Moreover, they have fewer side-effects. However, treatment is complicated by the fact that results are unpredictable; and in addition the side-effects that they do have can be very serious, such as diabetes, which in itself is life-threatening. However, as the potential side-effects are known, the physician has leeway to choose a drug which is a good match for the patient’s clinical profile. Then, once the patient’s symptoms have been much alleviated with an appropriate newer generation atypical antipsychotic, the patient should be able to also benefit from a range of psychotherapeutic interventions. It is argued that this is the best treatment regime to choose, as it is likely to result in the greatest improvement in quality of life, coupled with the lowest risk of potentially devastating side-effects, or of death. This is likely to be better than utilizing cognitive behavioral therapy, the results of which are not reliably known – although research has certainly shown that it is less efficacious

(2) However, there are some problems with this evidense. Amphetamines only mimic the positive symptoms of schizophrenia. They do not produce any of the negative symptoms. Likewise, anti-psychotic drugs are only affective on the positive symptoms of the disease. There is still some evidense that schizophrenics do posess higher levels of dopamine, however, these increases are only found in the striatum of the brain (7). The striatum is a region of the brain that receives its inputs from and outputs to the cortex. Injury to the striatum results in problems with intiation and control of motor behavior. (9) Also, there is evidence that the prefrontal cortex produces lower levels of dopamine. (4) The prefrontal cortex is involved in the organization and coordination of information to and from the cortex. (7)

A comparison between schizophrenia and bipolar spectrum disorder focusing on history, etiology, treatment, and symptoms of each disease will introduce the concept of the Continuum Disease Model (CDM) as a basis for further debate and discussion on the controversial designation of schizoaffective disorder (bipolar type/depressive type). The concept of a possible connection between distinct disorders is strongly disputed between many experts due to presence of manic or hypomanic episodes as a clear distinction requiring the designation of bipolar spectrum disorder as opposed to negative and positive schizophrenic symptoms; however, similarities in the disorders including etiology, presence of psychosis, and effectiveness of new atypical antipsychotic treatments may present similar neurological psychopathology. Schizoaffective disorder may present only unipolar depressive symptoms along with negative or positive schizophrenic symptoms but bipolar type will be the focus of discussion. An argument disputing the legitimacy of the CDM will be presented though the stress-diathesis model supports the designation of schizoaffective disorder in the newest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). A deeper look at the mechanisms in the psychopharmacological drug treatments specifically focused on the atypical antipsychotics quetiapine (trade name Seroquel) and lurasidone (trade name Latuda), providing theories of their effects on brain

While there is no cure for schizophrenia, research is leading to new, safer treatments. Experts also are unraveling the causes of the disease by studying genetics, conducting behavioral research, and by using advanced imaging to look at the brain’s structure and function. These novel approaches hold the promise of new, more effective therapies.

Schizophrenia is a life-long disorder that affects about one percent of the population (Mueser & McGurk, 2004). The cause of this mental illness is still unclear. Studies have suggested that Schizophrenia does not arise from one factor but from a combination of genetic, environmental, and social factors (Liddle, 1987). People diagnosed with Schizophrenia struggle to deal with a multitude of symptoms that make it difficult to function (Mueser & McGurk, 2004). Antipsychotic medications are a popular treatment of the symptoms of Schizophrenia (Mueser & McGurk, 2004). Research is constantly being done to develop these medications to enhance the quality of life of those diagnosed with Schizophrenia.