Genetics and Mental Health Disorder

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Genetics and Mental Health Disorder

Research continues to affirm the influence of genes in the development of mental illnesses such as depression, bipolar disorder, schizophrenia and autism. Mental illnesses have become crucial public health problems in the global spectrum, and current data in the United States necessitates the need to establish a strong understanding of risk factors, diagnosis, treatment, prevention and management.  Current developments in research establish the growing relationship between mental illnesses and genes, especially in a country like the United States, where the trajectory of risk exposure remains high. The Center for Disease Control and Prevention estimates that nearly half of adults (46.4%) will experience mental illness during their lifetime, while 5% of adults experience mental illness in any one year. These figures highlight the depth of mental diseases in the United States and the threats it presents to public health, demanding the need to understand the link between the genes.

Genetic alteration

The characterization of shared symptoms associated with mental disorders forms one of the fundamental basis for establishing the link with the genetic composition of individuals. Anttila et al. (2018) observe that brain disorders may manifest similar symptoms and strong epidemiological commodity that can directly be linked to etiologic overlap, inheritance and genetic alterations. The relationship between psychiatry disorders and the fact that they share similar variant risk opens the debate about the role of gene-phenotypes in increasing the risk to mental diseases aspects evaluated by Ruderfer et al. (2018) by identifying common symptoms of bipolar disorder and Schizophrenia and how they relate to DNMT1 alterations. Comparing Schizophrenia with bipolar disorder relative to the human genome establishes the existence of four genomic regions entailing one with disorder-independent causal variants and potassium ion response genes. Ruderfer et al. (2018) findings create a strong link between gene phenotypes alterations and development of severe psychiatric disorders.

Genetic alterations play critical roles increasing risk exposure to mental health disorders, and according to Hamidi et al. (2015), DNA methylation can cause changes to chromatin structure and gene expression. Discussions regarding DNMT mutations in human disease development remain controversial, but Jin & Liu (2018) explain how exome sequencing to establish the relationship between gene alteration and dementia. In DNMT mutations, patients’ patient development dementia as the structure of hereditary sensory and automatic neuropathy undergoes changes observations supported by Norvil et al. (2019) view in an analysis of DNMT1 homozygous deletion in mice. Jobe and Zhao (2017) underline that DNMT1 mutations identified in human patients increase the risk factor for neuro-generative diseases. Alzheimer's disease, for instance, occurs as results of defects in RAN (RAS-related Nuclear protein). In Román et al. (2019) view, alteration of nuclear transport of DNMT1 and RNA polymerase II expose individuals to manifests symptoms of Alzheimer disease.

Talkowski et al. (2011) advance the knowledge of neurodevelopmental disorders by the assertion of how autism spectrum disorder harbors chromosomal microdeletions. Development and exposure rate to autism spectrum disorder increases with alterations or deletion in chromosomes associated with mRNA expression (Krol et al., 2018). Alteration such as partial deletions of noncoding regions induces intellectual disability, epileptic symptoms and features related to autism. In Talkowski's et al. (2011) observations genetic alterations of methyl- CpG-binding domain 5 (MBD5) triggers features of 2q23.1 microdeletion syndrome which plays an essential role in the development of Autism Spectrum Disorder (ASD) findings support by Williams et al. (2010). According to Williams et al. (2010), microdeletion of chromosome 2q23.1 leads to increased exposure neuro-generative syndromes, especially those associated with developmental and cognitive delays. Chromosomal deletion results in impaired speech, short stature, behavioral disorders and sometimes seizures, symptoms directly related to mental diseases such as Autism Spectrum Disorder and Alzheimer.

Romer et al. (2018) discuss the general liability factors for psychopathology and risk factors that contribute to mental disorders. Although the Romer et al. (2018) appreciates increased research in mental health, gaps remain wide, especially in terms of understanding specific genotype alterations that trigger mental illnesses. Romer et al. (2028) findings suggest that structural changes in corticocerebellar circuitry responsible for enhancing core brain functions such as coordination and information management contribute to the development of mental disorders. Increase incidence of depression in the world attracts, and the disorder, which affects nearly 300million annually has been identified to be triggered by alteration of the gene known as Slc6a15, whose primary role entails stress regulation. UM SOM (2017) establishes that people with altered levels of Slc6a15 genes in specific brain regions have higher risk exposure to depression and other emotional illnesses related to stress.

 Neural circuits are associated with mental health functions.

Besides increased research on specific gene alterations and their leads in the development of mental health disorders, further studies have attempted to identify specific neural circuits that are involved in mental illness. Understanding particular neural circuits in disease pathophysiology enhance the frameworks for diagnosis, prevention and treatment and to Dunlop et al. (2017), there are numerous neural circuits associated with mental illnesses. The default mode circuit is strongly related to depressive disorder. Di et al. (2018) observe that disruptions of grey and white matter in the default mode circuit through hyperactivity or function can trigger depression among individuals. In further analysis, Peters et al. (2016) observe the role of the Salience circuit cognitive control and potential role in triggering mental disorders. The Salience circuit primarily functions by detecting alterations in the environment and signal processes and initiation of cognitive control and may affect behaviour or induce stress. Winton-Brown et al. (2017) findings on the role of the Salience circuit in mental health disorders is supported by Liberzon & Abelson (2016) who notes that Insula hypo-connectivity within the salience circuit contributes to high-risk exposure to social anxiety, panic disorder and depression. 

Schulze et al. (2019) evaluate the role of negative affect neural circuit in appraisal and expression of emotions. The dysfunction of the adverse affect neural circuit directly induces subjective mood and negative expression of emotions. In support of Schulze et al. (2019) views regarding the role of negative affect neural circuit in mental illness development, Young et al. (2017) affirm that through insula activation individuals are likely to develop a depressive disorder or social anxiety disorder.  Further analysis suggests that hyper-connectivity with the negative affect circuit involving anterior nodes triggers depression. The role of attention circuit in mental health illnesses mostly increase risk exposure to anxiety disorder, and according to Martínez et al. (2016) front parietal circuit hypo-connectivity within the attention, the circuit can induce behavioural tendencies of false alarm associated with fear and anxiety. Williams (2016) further evaluates how cognitive control circuit comprising of dorsolateral prefrontal cortex and dorsal parietal cortex play roles in creating risk exposure to depressive disorders, bipolar disorders and anxiety.

Lesh et al. (2010) link deficits in the cognitive control circuit to development of Schizophrenia, assessing that functional abnormalities and cognitive dysfunction within the circuit contribute to the pathophysiology of elevated cognitive deficit in Schizophrenia. According to Ray et al. (2017), cognitive control is a cognitive and neural mechanism that plays a crucial role in managing complex functions and tasks in individual day-to-day lives. Functional impairments in cognitive control neural circuit, however, has the potential of creating cognitive deficit associated with Schizophrenia (Pirnia et al., 2015).

Assessing the shared molecular neuropathology across major mental health disorders, Gandal et al. (2018) establishes that genetic variants and deficits in neural circuits induce brain dysfunction or pathology implicit on development of disorders such as autism, bipolar and depression. In a comprehensive assessment regarding predisposition to neuropsychiatric diseases, Gandal et al. (2018) identified patterns of shared and unique gene-expression perturbations across the mental health illnesses. The findings are supported by Fromer et al. (2016) through assessment of cognitive circuit deficit that harbours Schizophrenia—observing the development of Schizophrenia, Fromer et al. (2016) advance the efforts to understand the role of genetic variants as critical risk factors. The genetic basis for the risks of Schizophrenia lies on the identification of the rare copy-number variants and according to Fromer et al. (2016) gene co-expression implicates neural networks that contribute to high-risk exposure to Schizophrenia.

 Genetic research on neurobiology and mental health

Existing diagnostic approaches for mental health illnesses rely significantly upon observation of presenting signs and symptoms, a dimension Yahata et al. (2017) suggests to be inadequate in establishing treatment, prevention and recovery options. Genetic research present opportunities for understanding the etiology and pathophysiology of mental disorders and the National Institute of Mental Health recognize the importance of genetics in understanding mental health disorders. Studying the case of Bipolar disorder, Harrison et al. (2018) demonstrate the increasing role of neurobiology research in diagnosis and treatment of mental health disorders. Bipolar disorder, for instance, is highly heritable and attributed to a common variant of small effects. Understanding the options of neural transmission defects would allow specific approach in diagnosis based on factors outside presenting symptoms. Harrison et al. (2018) look at the role of calcium signalling in the development of therapeutic traction underlining the necessity of research in neurobiology as part of solution development against mental health diseases.  Increased research into the area of neurobiology relative to mental illnesses promotes the understanding of neural circuitry involve cognitive control, negative affect and positive affect circuits.

Understanding elements of cognitive dysfunction associated with mental illnesses should be the priority setting of neurobiology. According to Rodrigue et al. (2018), studies in Schizophrenia continue to use neuropsychological elements to understand different aspects of cognition in disorders and form part of establishing existing neural deficits that initiate mental instability. Since mental illnesses affect neural, cognitive abilities, it is imperative to harness diagnosis and treatment interventions around neural behaviors of patients. Research in neurobiology will enhance treatment discoveries through understanding the establishment of how the human brain functions and the mechanisms involved. Yahata et al. (2017) escalate the idea that neurobiology enhances the ability to understand behavioral responses associated with mentally ill patients besides promoting awareness on sensory and motor information in the human brain, and how that affects prevention, treatment and recovery. Neurobiology role in the fight against mental health emphasizes on targeting and remedying the source of the problems besides the fact that it promotes early diagnosis. According to Rose (2016), neuroscience forms the future of diagnosis, treatment and prevention of mental illnesses, fostering the idea that it will allow early interventions.