• Korean Journal of Biological Psychiatry
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• v.18 no.4
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• pp.176-180
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• 2011

Depressive disorders have strong genetic components. However, conventional linkage and association studies have not yielded definitive results. These might be due to the absence of objective diagnostic tests, the complex nature of human behavior or the incomplete penetrance of psychiatric traits. Imaging genetics explores the influences of genetic variation on the brain function or structure. This technique could provide a more sensitive assessment than traditional behavioral measures in psychiatric studies. Imaging genetics is a relatively new field of psychiatric researches, and may improve our understanding on neurobiology of psychiatric disorders. In this review, current understanding in neurobiology of depressive disorders, especially imaging genetic studies on serotonin transporter will be discussed.

• Korean Journal of Biological Psychiatry
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• v.1 no.1
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• pp.60-66
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• 1994

Advances in molecular biology have renewed hope for the discovery of disease relevant gene. The basic strategy is gene mapping and likely to have on important role in psychiatric research and practice. Recent linkage studies of chromosomal loci to psychiatric diseases shed light on the potential for new genetics in psychiatric science. This article reviews molecular application to psychiatrymethodological issues in genetic linkage, study of gene expression by analysis of mRNA, and current linkage studies in psychiatric diseases.

• Korean Journal of Biological Psychiatry
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• v.7 no.2
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• pp.123-130
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• 2000

The development of inexpensive high throughput methods to identify individual DNA sequences is important to the future growth of medical genetics. This has become increasingly apparent as psychiatric geneticists focus more attention on the molecular basis of complex multifactorial diseases at which most of psychiatric disease is estimated. Furthermore, candidate gene approaches used in identifying disease associated genes necessitate screening large sequence blocks for changes tracking with the disease state. Even after such genes are isolated, large scale mutational analysis will often be needed for risk assessment studies to define the likely medical consequences of carrying a mutated gene. This review provide basic knowledge of up-to-date technology, cDNA microarray which enables above mentioned various research themes.

• Genomics & Informatics
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• v.2 no.1
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• pp.1-6
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• 2004

• Korean Journal of Biological Psychiatry
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• v.23 no.3
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• pp.69-79
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• 2016

Frontotemporal dementia (FTD) is a degenerative disease characterized by the selective frontal and temporal lobe atrophy, and progressive deficits in behavior, executive function, or language. The prevalence and incidence of FTD are 15-22/100000 and 2.7-4.1/100000, respectively, in midlife. Hereditary is an important risk factor for FTD. Although there is some controversy regarding the further syndromatic subdivision of the different types of FTD, FTD is clinically classified into behavioral variant of frontotemporal dementia, semantic dementia and progressive nonfluent aphasia. FTD can be misdiagnosed as many psychiatric disorders because of similarity of the prominent behavioral features. Advances in clinical, imaging, and molecular characterization have increased the accuracy of FTD diagnosis, thus developing for the accurate differentiation of these syndromes from psychiatric disorders. We also discuss about therapeutic strategies for symptom management of FTD. Medications such as serotonin reuptake inhibitors, antipsychotics, and other novel treatments have been used in FTD with various rates of success. Further advanced research should be directed at understanding and developing new diagnostic and therapeutic modalities to improve the FTD patients' prognosis and quality of life.

• Korean Journal of Biological Psychiatry
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• v.19 no.1
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• pp.29-37
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• 2012

The loudness dependence of the auditory evoked potential (LDAEP) has been proposed as a valid biomarker of central serotoninergic activity in humans. The specificity and sensitivity of the LDAEP to changes in serotonergic neurotransmission have recently been explored in many studies about pharmacology and genetics. The majority of evidence for an association between the LDAEP and serotonin activity has come from animal studies. Genetic association studies with the LDAEP have provided conflicting reports with additional evidence outlining sensitivity to other neurotransmitter systems including the dopamine and glutamatergic systems. The LDAEP has been revealed to reflect the pathophysiology of various psychiatric illnesses. There is supporting evidence that major psychiatric disorders have differential LDAEP activities. Overall, the LDAEP shows strong evidence as a potential predictor of antidepressant treatment response. It need to be explored whether the LDAEP could be a biological marker of various psychiatric diseases and treatment prediction of antidepressants and serotonin related drugs.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.16 no.1
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• pp.5-14
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• 2005

There has been an enormous progress in understanding of how genes contribute to both normal and abnormal development. Also many laboratory works are exploring the intricacies of how to develop in the human central nervous system. Understanding the mechanisms of cortical development gives essential insight into the pathogenesis of many genetic and acqured developmental psychiatric disorders, including autism, schizophrenia, and teaming disorder. Genes have been implicated in an ever-increasing number of disorders. Advance in genetics have begun to clarify the molecular basis of not only single-gene disorders, but also more complex phenotypes.

• Korean Journal of Biological Psychiatry
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• v.5 no.1
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• pp.17-33
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• 1998

Advances in molecular biology contribute to the understanding genetic mechanism of psychiatric disorders. They have renewed hope for the discovery of disease relevant gene. However, the results somewhat confused. And we will wait for a long time for the application of gene therapy in schizophreniar. Fortunately we could classified the schizophrenia with genotypes of dopamine and serotonin receptors. It is expected that this genetic classification could provide key strategy for the therapeutic application in biological treatment for schizophrenia. The purpose of this article is to call attention of the institute participants to linkage, association, mRNA expression, genotypic classification and to the need for more systemic research. The author summarized the modified methods which were done in his laboratory in appendix.

• Sleep Medicine and Psychophysiology
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• v.20 no.2
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• pp.53-58
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• 2013

Autism Spectrum Disorder (ASD) is characterized by persistent deficits in social communication and restricted, repetitive patterns of behavior and interest. Sleep problems are not uncommon in children with autism spectrum disorders. Symptoms of insomnia are the most frequent sleep problems in individuals with ASD. Sleep problems can cause significant difficulties in the daily life of children with ASD and their families. Genetic factor, deregulations of melatonin synthesis, extraneous environmental stimuli and psychiatric and medical conditions may cause sleep problems. The first line treatment of sleep problems in ASD includes managements for potential contributing factors and parent education about sleep hygiene care for child and behavioral therapy. Supplementation with melatonin may be effective before considering other medications, such as risperidone, clonidine, and mirtazapine.

• Clinical and Experimental Pediatrics
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• v.54 no.2
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• pp.55-63
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• 2011

Prader-Willi syndrome (PWS) is a complex multisystem genetic disorder that is caused by the lack of expression of paternally inherited imprinted genes on chromosome 15q11-q13. This syndrome has a characteristic phenotype including severe neonatal hypotonia, early-onset hyperphagia, development of morbid obesity, short stature, hypogonadism, learning disabilities, behavioral problems, and psychiatric problems. PWS is an example of a genetic condition caused by genomic imprinting. It can occur via 3 main mechanisms that lead to the absence of expression of paternally inherited genes in the 15q11.2-q13 region: paternal microdeletion, maternal uniparental disomy, and an imprinting defect. Over 99% of PWS cases can be diagnosed using DNA methylation analysis. Early diagnosis of PWS is important for effective long-term management. Growth hormone (GH) treatment improves the growth, physical phenotype, and body composition of patients with PWS. In recent years, GH treatment in infants has been shown to have beneficial effects on the growth and neurological development of patients diagnosed during infancy. There is a clear need for an integrated multidisciplinary approach to facilitate early diagnosis and optimize management to improve quality of life, prevent complications, and prolong life expectancy in patients with PWS.