What are most hypotheses regarding the etiology of schizophrenia?
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The etiology of schizophrenia is multifaceted, with various hypotheses proposed. Genetic factors play a significant role, as indicated by twin, family, and adoption studies, with neurodevelopmental genes like BDNF, NT-3, NCAM, synapsin, and SNAP-25 being of interest . Dopaminergic and serotonergic theories have guided current therapies, while the NMDA receptor hypofunction hypothesis suggests a more complex underlying cause . Biochemical theories focus on neurotransmitters like dopamine, glutamate, serotonin, and acetylcholine, with neurodevelopmental and neurodegenerative causes gaining support . Recent advances in genetics through GWAS, CNVs studies, and exome sequencing have led to new hypotheses on the genetic basis of schizophrenia . Additionally, the involvement of herpes simplex virus type 1 and human cytomegalovirus, along with immunoglobulin GM genes, has been linked to cognitive impairment in schizophrenia patients, suggesting viral and genetic influences .
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Open access•Journal Article | The paper mentions that there are many hypotheses on the etiology of schizophrenia, including biochemical theories related to unbalanced chemical substances in the brain and neurodevelopmental and neurodegenerative causes. |
3 Citations | The neurodevelopmental hypothesis, focusing on genetic factors affecting brain development, is a prominent theory in schizophrenia etiology, supported by studies on neurotrophic factors, NCAM, synapsin, and SNAP-25. |
3 Citations | The paper discusses the hypothesis that common immunoglobulin γ genes may be potential risk factors for schizophrenia. |
Open access•Dissertation 13 May 2020 | The dopamine hypothesis and NMDA receptor hypofunction hypothesis are key etiological theories for schizophrenia, highlighting neurotransmitter dysregulation. Current research focuses on their interplay for deeper insights. |
Open access•Journal Article 1 Citations | Genetic variants, genome-wide association studies (GWAS), copy number variations (CNVs), and exome sequencing have led to new hypotheses about the etiology of schizophrenia, indicating future research directions. |
Related Questions
What are the causes of schizophrenia in children?5 answersThe causes of schizophrenia in children can be attributed to a combination of genetic and environmental factors. Genetic factors play a significant role, with genes like ErbB4, DTNBP1, NRG1, dopamine, and COMT being implicated in the pathogenesis of the disorder. Neurodevelopmental abnormalities, such as disruptions in neuronal development during critical periods like adolescence, can lead to impairments in cognitive functions and emotion regulation, contributing to the onset of schizophrenia in children. Additionally, neuroimaging studies have shown structural abnormalities in the brain, including decreased cortical gray matter, altered white matter connectivity, and deficits in subcortical areas, which may underlie the cognitive and social skill deficits observed in childhood-onset schizophrenia. Early identification and intervention are crucial in managing the complex nature of schizophrenia in children.
What are some of the environmental factors affecting schizophrenia?4 answersEnvironmental factors that have been identified as affecting schizophrenia include urbanicity, air pollution, and exposure to green spaces. Growing up in an urban environment has been linked to changes in brain development, particularly in the dorsolateral prefrontal cortex and the perigenual anterior cingulate cortex. Air pollution, specifically exposure to particulate matter, gases, organic compounds, and metals, can lead to neurotoxicity and neuropathology, potentially increasing the risk of schizophrenia. On the other hand, higher exposure to green spaces has been suggested to reduce the incidence of schizophrenia, with a dose-response association between childhood exposure to green space and a lower risk of developing the disorder in the future. Other environmental factors that have been studied include obstetric complications, infections, childbirth in the winter or spring, severe childhood events, and marijuana use. These factors, along with genetic risk factors, interact to increase the risk of developing schizophrenia.
What are the hypotheses of schizophrenia?5 answersThe hypotheses of schizophrenia include the dopamine hypothesis, the glutamate hypothesis, the GABA hypothesis, and the NMDA receptor hypofunction hypothesis. The dopamine hypothesis suggests that abnormalities in dopamine transmission contribute to the development of schizophrenia. The glutamate hypothesis proposes that dysfunction in glutamate neurotransmission, particularly involving NMDA receptors, is involved in the pathophysiology of schizophrenia. The GABA hypothesis suggests that alterations in GABAergic signaling may contribute to the development of schizophrenia. The NMDA receptor hypofunction hypothesis suggests that dysfunction in NMDA receptors, which are involved in glutamate neurotransmission, plays a role in the development of schizophrenia. These hypotheses provide insights into the underlying molecular mechanisms of schizophrenia, but further research is needed to fully understand the complex nature of the disorder.
What are the genetic factors that contribute to schizophrenia?4 answersGenetic factors that contribute to schizophrenia include polymorphic non-reference transposable elements (nrTEs). These mobile genetic elements make up half of the human genome and have been found to possibly contribute to the emergence of schizophrenia through a cis-regulatory effect. In addition, variations in gene expression features, such as differentially expressed genes (DEGs) and co-expression networks, have been associated with the heritability of schizophrenia. DEGs have been shown to be associated with the genetic risk of schizophrenia in a cell type-specific manner and are enriched for target genes of schizophrenia-associated transcription factors. Furthermore, rare tandem repeat expansions (TREs) have been found to be more prevalent in individuals with schizophrenia and are located near exons and at loci associated with schizophrenia. These TREs may impact synaptic functions by disrupting gene splicing. Overall, these genetic factors contribute to the polygenic nature of schizophrenia.
What are the molecular mechanisms of schizophrenia?4 answersThe molecular mechanisms of schizophrenia involve abnormalities in multiple epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs. Transcriptome studies have revealed synaptic, mitochondrial, immune system, gamma-aminobutyric acidergic, and oligodendrocytic changes as integral parts of the disease process. Schizophrenia susceptibility genes impact common intracellular signaling pathways, such as AKT, calcineurin, and DISC1, which regulate protein phosphorylation, dephosphorylation, and signaling cascades. Neuroepigenetic studies have shown dysregulated expression of synaptic and metabolic genes in schizophrenia brain, potentially linked to genetic risk architecture and environmental exposures. Metabolomic analysis has identified altered levels of amino acids and lipids in schizophrenic patients, suggesting potential biomarkers for diagnosis. These findings highlight the complex nature of schizophrenia, involving epigenetic modifications, disrupted signaling pathways, and metabolic abnormalities.
What is the pathophysiology of schizophrenia?5 answersThe pathophysiology of schizophrenia involves a complex interplay of genetic and environmental risk factors, leading to impairments in cognition, perception, emotions, social function, and behavior. Neurodevelopmental derailments and synaptic refinements during early development and adolescence contribute to the disorder. Dopaminergic and other neurotransmitter aberrations, particularly in glutamatergic neurons, are involved in the pathophysiology. Gray and white matter changes, with gray matter changes being more significant after the onset of psychosis, are observed in patients with schizophrenia. These structural alterations may contribute to impairments in executive functioning, attention, and working memory. The disease can be managed with pharmacological treatments based on individual patient profiles, compliance, and disease severity. Further understanding of the pathological processes and molecular mechanisms of synaptic plasticity, influenced by disease-risk genes and environmental alterations, will advance our understanding of schizophrenia.