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How Does Schizophrenia Affect The Nervous System

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How Does Schizophrenia Affect The Nervous System – In the largest study of its kind to date, 160 scientists from 27 institutions around the world decided to investigate how schizophrenia affects the brain’s white matter, a fatty substance found in brain tissue. brain.

To this end, the researchers analyzed the data obtained on about 2,000 people with schizophrenia, comparing it with data on more than 2,300 healthy controls.

How Does Schizophrenia Affect The Nervous System

The researchers looked at the brain’s white matter, which can be found in the brain’s subsurface. The white matter contains nerve fibers, which are protected by encasing them in a myelin sheath.

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Information from the new study was gathered from 29 existing studies by Improving Neurobiology through Meta Analysis.

ENIGMA is directed by Paul Thompson of the Neuroimaging and Informatics Center at the Keck School of Medicine’s Center for Neuroimaging and Informatics, part of the University of Southern California (USC), Los Angeles.

Neda Jahanshad, who is an assistant professor of physiology in the Center for Neuroimaging and Informatics at USC, along with Sinead Kelly, a researcher at the Keck School of Medicine in the USC Center for Neuroimaging and Informatics. .

Kelly and her colleagues used data from diffusion tensor imaging, a type of magnetic resonance neuroimaging that allows researchers to determine the location and alignment of fibers in the white matter of the brain.

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Research shows that schizophrenia affects the entire brain’s communication system, not just individual areas.

“For the first time, we can say with certainty that schizophrenia is a disease that affects the white matter in the brain. Sinead Kelly

However, two areas of the brain were found to be more affected than others. One is the part of the brain known as the corpus callosum, which allows the two parts to communicate with each other, and the other is the front part of what is called the coronal radiation, which is where the brain processes information. . .

, who proposed that schizophrenia is caused by a disorder that occurs only in the frontal and temporal lobes. These are the parts of the brain that regulate behavior, decision making, and auditory perception.

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“Without this research, future research could be wrong […] Instead of looking for genes that affect a ‘part of the wire,’ researchers will now look for genes that affect the entire network of the brain. ” Prof. Not Jahanshad

“We’ve shown that just looking at one area of ​​the brain to find out what causes schizophrenia is not a good way,” she said.

“The impact is global. Focusing on one area of ​​the brain where you think the effect will occur won’t tell you the whole story.

“Our research,” said Kelly, “will help to understand the mechanisms of schizophrenia, a mental disorder that, if left untreated, often leads to unemployment, homelessness, alcoholism, and even suicide.”

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In fact, the US Department of Housing and Urban Development estimates that 26 percent of homeless people living in shelters suffer from a “serious mental illness such as schizophrenia.”

“These findings,” said Kelly, “may help identify biomarkers that allow researchers to test patients’ response to schizophrenia treatment.”

The next steps related to this study include investigating the reasons for the observations made in this study. Kelly points to the hereditary nature of the disease, pointing out that certain genes can change the entire wiring of the brain.

, in fact, recently reported a major study that confirmed that 80 percent of the risk of schizophrenia is genetic. Brain dysfunction in schizophrenia: Combination of genetic and environmental risk factors leading to impaired neuroinflammation.

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Schizophrenia is a disease of heterogeneous etiology involving a complex interaction of genetic and environmental risk factors. The immune system is now known to play an important role in nervous system function and pathology, regulating neuronal and glial structure, synaptic plasticity, and behavior. In this regard, the immune system is a common link between factors that appear to differentiate genetic and environmental risk factors for schizophrenia. To better understand the pathogenesis of this disease, it is necessary to gather information about how many factors affect the immune-brain axis and how these factors can interact in schizophrenia. Such knowledge will lead to the development of translatable animal models that may lead to more effective therapies. Here, we provide an overview of molecular risk factors for schizophrenia that modulate immune function. We are also investigating environmental risk factors for schizophrenia, including pollution, gut dysbiosis, maternal immune activation, and early stress, and how the effects of these risk factors affect microglial function and dysfunction. We also suggest that the disruption of signaling in the blood brain barrier observed in some people with schizophrenia may act as a gateway between peripheral and central inflammation, thus affecting microglia in their basic functions. In conclusion, we describe the different roles that microglia play in response to neuroinflammation and their implications for brain development and homeostasis, as well as the pathogenesis of schizophrenia.

Schizophrenia (SCZ) is a psychiatric disorder that does not require adequate treatment. Approximately 20 million people worldwide suffer from this mental illness (American Psychiatric Association, 2013; Whiteford et al., 2013). SCZ has a variety of symptoms, including hallucinations, social and cognitive impairment, and thought and behavioral disturbances that interfere with daily functioning (American Psychiatric Association, 2013 ). Current treatment options do not improve cognitive function or negative symptoms, both of which contribute more to SCZ long-term prognosis than positive symptoms (Lieberman et al., 2005; Green, 2006). Effective treatments for SCZ have lagged behind due to a lack of understanding of its mechanisms.

Genome-wide association studies (GWAS) have identified a new susceptibility gene that increases the risk of SCZ (Ripke et al., 2013; Li et al., 2017). These advances have led to genetic characterization that may shed light on the pathogenesis of SCZ. In addition, there has been significant progress in research specifically focusing on environmental risk factors for SCZ and other neurodevelopmental disorders (NDDs) that alter brain development, such as psychosocial stress, activation maternal immunity (MIA), and exposure to pollution (Bergdolt and Dunaevsky). , 2019; Gomes et al., 2019; Horsdal et al., 2019). Although there are a number of genetic and environmental factors that contribute to the increased risk of SCZ, recent work has shown that these factors combine to alter the immune system known to play an important role in brain development (Müller and Schwarz, 2010; Stephan et al., 2012). ; Kroken et al., 2018). Indeed, SCZ is associated with enhanced immune function and chemokine responses, and drugs targeting immune function have shown some success in reducing symptoms (Sommer et al., 2014; Frydecka et al., 2018; Kroken et al. , 2018). Importantly, subclinical inflammation correlates with cognitive impairment in SCZ (Misiak et al., 2018), which is an important predictor of long-term prognosis in this disease. How antibodies control synaptic wiring during normal brain development and contribute to synaptic pathology in neuropsychiatric disorders is unknown. Links between specific immune cells and altered synaptic connectivity in circuits associated with neuropsychiatric disorders are currently lacking (Elmer and McAllister, 2012).

Microglia are central nervous system (CNS) phagocytes that, among their other functions, regulate innate immunity in the brain. Microglia have a well-defined role in the rapid response to inflammatory insults, the dynamic maintenance of the parenchyma of the CNS (Nimmerjahn et al., 2005; Liu Y. U. et al., 2019) and the clearance of debris and apoptotic cells through phagocytosis (Ayata et al., 2018). Galloway et al., 2019). Recent research has begun to reveal the diversity of microglia, which can have different levels of gene expression in different regions of the brain, in health and disease, and at different times. different developmental stages (Tay et al., 2017a; Hammond et al., 2019). Sankowski et al., 2019; Tan et al., 2020). These complex cells contribute to normal brain development and function by supporting neuronal circulation through synapse addition, removal, maintenance, and plasticity (Hammond et al., 2018; Bohlen et al., 2019). Despite differences in findings from several studies, there is evidence for microglial dysfunction in SCZ (Bayer et al., 1999; Hercher et al., 2014; Bloomfield et al., 2016; Trépanier et al., 2016; De Picker et al., 2017; Sellgren et al., 2017). et al., 2019; Uranova et al., 2020). A key factor in understanding the pathogenesis of SCZ is elucidating how genetic and environmental risk factors interact to alter microglial function. Furthermore, at what stage(s) of disease progression does microglial function improve or contribute to the pathogenesis of SCZ, and what are the specific microglial subtypes or phenotypes that can be targeted? for therapeutic purposes.

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In this review, we discuss the genetic and environmental risk factors associated with SCZ and how they combine to alter microglial function in response to systemic and central inflammation. Additionally, we highlight how these risk factors alter critical microglial functions during development, adolescence, and adulthood. It also explores the limitations of current knowledge and suggests major future experiments. Understanding how different organisms and

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