This Research Topic is the second volume of Research Topic "Molecular Mechanisms of Neuropsychiatric Diseases". Please see the first volume
here.
Psychiatric diseases, such as depression, schizophrenia, bipolar disorder, obsessive compulsive disorder, post-traumatic stress disorder (PTSD) and autism spectrum disorder, are estimated to impair 350 million individuals globally. The likelihood of developing psychiatric disorders depends on a variety of both genetic and environmental factors. For some disorders, such as PTSD, an environmental insult is easily identified, while for other disorders, such as schizophrenia, it is likely a gene x environment interaction where the environmental insult may be less apparent. Ongoing work in the field of psychiatric neuroscience is aimed at elucidating the molecular mechanisms underlying these and other psychiatric conditions. For example, by the early 2000s, dendritic spines and NMDA receptors had been implicated in schizophrenia pathology. Furthermore, a relationship between stress hormones and PTSD has been established by studies demonstrating that PTSD patients show an increase of the stress hormones norepinephrine and epinephrine in urine. Gene expression and translation have also been extensively studied in human post-mortem brain tissue from subjects with psychiatric disease.
The goal of this Research Topic is to explore the molecular mechanisms underlying neuropsychiatric diseases and how these mechanisms can be exploited for potential therapeutic benefit. For example, the DBH inhibitor nepicastat has an effect consistent with a decrease in the persistence of traumatic memories and anxiety-like behaviours in PTSD mice model. The disruption of traumatic memories may be important to decrease PTSD symptoms and signs. Furthermore, studies in live patients and of post-mortem brain tissue have found impairments in discreet brain areas, circuits and cellular structures that could potentially underlie disease symptoms in psychiatric diseases. By furthering our understanding of the mechanisms underlying these disorders we have the potential to uncover therapeutic targets and improve the quality of life of these patients.
Areas of interest for this Research Topic include but are not limited to:
• The molecular mechanisms underlying the persistence of contextual memories in PTSD
• Post-translational modifications in the aetiology of neuropsychiatric diseases for example, phosphorylation, glycosylation, and ubiquitination
• Potential therapeutics in neuropsychiatric diseases which exploit molecular mechanisms
This Research Topic is the second volume of Research Topic "Molecular Mechanisms of Neuropsychiatric Diseases". Please see the first volume
here.
Psychiatric diseases, such as depression, schizophrenia, bipolar disorder, obsessive compulsive disorder, post-traumatic stress disorder (PTSD) and autism spectrum disorder, are estimated to impair 350 million individuals globally. The likelihood of developing psychiatric disorders depends on a variety of both genetic and environmental factors. For some disorders, such as PTSD, an environmental insult is easily identified, while for other disorders, such as schizophrenia, it is likely a gene x environment interaction where the environmental insult may be less apparent. Ongoing work in the field of psychiatric neuroscience is aimed at elucidating the molecular mechanisms underlying these and other psychiatric conditions. For example, by the early 2000s, dendritic spines and NMDA receptors had been implicated in schizophrenia pathology. Furthermore, a relationship between stress hormones and PTSD has been established by studies demonstrating that PTSD patients show an increase of the stress hormones norepinephrine and epinephrine in urine. Gene expression and translation have also been extensively studied in human post-mortem brain tissue from subjects with psychiatric disease.
The goal of this Research Topic is to explore the molecular mechanisms underlying neuropsychiatric diseases and how these mechanisms can be exploited for potential therapeutic benefit. For example, the DBH inhibitor nepicastat has an effect consistent with a decrease in the persistence of traumatic memories and anxiety-like behaviours in PTSD mice model. The disruption of traumatic memories may be important to decrease PTSD symptoms and signs. Furthermore, studies in live patients and of post-mortem brain tissue have found impairments in discreet brain areas, circuits and cellular structures that could potentially underlie disease symptoms in psychiatric diseases. By furthering our understanding of the mechanisms underlying these disorders we have the potential to uncover therapeutic targets and improve the quality of life of these patients.
Areas of interest for this Research Topic include but are not limited to:
• The molecular mechanisms underlying the persistence of contextual memories in PTSD
• Post-translational modifications in the aetiology of neuropsychiatric diseases for example, phosphorylation, glycosylation, and ubiquitination
• Potential therapeutics in neuropsychiatric diseases which exploit molecular mechanisms
