Neurotransmitter dysfunction and genetic risk in schizophrenia

How to better decode and formulate appropriate treatment plans has long been an important topic that has attracted researchers in fields as diverse as neuroscience and psychiatry. As we all know, as a serious mental illness, its pathogenic factors and pathological features are complicated, which makes it easy to be misdiagnosed. furthermore, the functional impairment of the disease seriously reduces the quality of life of patients. However, as more scientific research has unfolded, there is overwhelming evidence that chemical imbalances in the brain and genetic risks are important causes of schizophrenia. In this article, we provide an in-depth analysis of neurotransmitter dysfunction and genetic risk in schizophrenia based on two summaries of the well-referenced schizophrenia research literature. First, we review the traditional view of neurotransmitter risk, the validity of new theories, and the possibility of multiple treatment modalities. Second, clues from genetic theories such as the selfish gene theory and imprinted genes were examined, adding new insights into understanding genetic risk. Studies have shown that the potential risk factors for schizophrenia are complex and that the glutamate theory can be a good remedy for the limitations of the traditional dopamine theory. Second, the genetic risk of this disorder can be explained by genetic tug-of-war and imprinted genes, with overexpression leading to extreme outcomes (abnormal symptoms). In this study. we identified the importance of genetic risk and neurotransmitter imbalance in schizophrenia and why refining these theories is important for decoding and treating schizophrenia.