Wednesday, May 6, 2020

The Pathophysiology And Etiology Of The Disease - 1420 Words

Abstract Schizophrenia effects approximately 1% of the human population, despite the high number of individuals being affected, not much is known about the pathophysiology and etiology of the disease. Through the use of pharmacological models such as ketamine and amphetamine, it allows us to purse the dopamine and glutamate hypothesis. The rise of these hypotheses is due to the nature of the disease, hence heterogeneous disorder not all patients exerts all the symptoms of the disease. As a result there is different ways in attaining schizophrenic animal models. One way is through ketamine administration which affects glutamate NMDA receptors. Another way is through amephetamine which increases the level of dopamine which affects the D ¬2†¦show more content†¦1. Introduction Animal models have been used as a primary research tool in investigating pathogenesis and developing treatments for human diseases. To mimic neuropsychiatric disorders in animal models, especially in the case of a complex disorders such as schizophrenia have been a tough task. This challenge persists due to the uncertainty of the pathophysiology and etiology that is presented with the disease. In addition to the unpredictability of the manifestation of the disease, symptoms that do occur in humans cannot be directly correlated with animal models. This presents a challenge where symptoms cannot be directly measured in animals more precisely in rodents. Despite the challenges that were present, researchers have went on forth to examine the disease using subtle approaches. Hence rodents don’t naturally develop schizophrenia, scientists must induce this through pharmacological, genetic, or environmental manipulations. The tools that are most used in pharmacological manipulations t o induce schizophrenia are: ketamine and amphetamine. In this perspective, we will focus on how reliable pharmacological manipulations are in construct validity, face validity and predictive validity in respect to ketamine and amphetamine. Understanding the validity of the animal models will help understand the pathogenesis of the disease and bring novel insights for treatment. The sooner we construct a better representable model of schizophrenia, it

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