• Korean Journal of Biological Psychiatry
• /
• v.19 no.1
• /
• pp.1-8
• /
• 2012

The mechanism of psychotherapy is explained by the recent developments in neuroscience and neuroimaging. The purpose of this study is to understand the nature of psychotherapy and to discuss the future of psychotherapy improvement with the help of advances of the neurobiological findings in psychotherapy. For this study, we investigated a wide range of materials. We searched for various researches on psychotherapy, brain, and neurobiology. In addition to the conventional psychodynamic psychotherapy, we investigated research findings on cognitive behavioral therapy, interpersonal psychotherapy and eye movement desensitization and reprocessing (EMDR). Moreover, based on the actual experiences of treating patients, we speculated the neurobiological mechanisms of the process and results of psychotherapy. With the development of neuroscience, we are now able to understand the personal consciousness, unconsciousness and developmental process. Also subdividing the disease is made possible. Personalized treatment has become available, and we are able to predict the prognosis of patients. Our memories are composed by implicit memory and explicit memory. By psychotherapy, we can consciously remember explicit memory, and it becomes easier to explore implicit memory through free association. Through psychotherapy, we will also be able to learn the effect of acquired environment and experience. Psychotherapy is able to correct human behaviors by modifying the memories. Through the regulation of emotions, it becomes possible to modify the memories and correct the behaviors. In this process, doctor-patient relationship is the main factor which cause positive treatment effects. Furthermore imagination therapy or unconscious, non-verbal stimuli could bring about positive treatment effects. Now psychotherapy could be explained and studied by neuroscientific researches. In this sense, we could provide the direction of future advances in neuroscience by the neurobiological understanding of psychotherapy.

• Clinical and Experimental Pediatrics
• /
• v.49 no.4
• /
• pp.341-353
• /
• 2006

Learning disorders are diagnosed when the individual's achievement on standardized tests in reading, mathematics, or written expression is substantially below that expected for age, schooling, and level of intelligence. Subtypes of learning disorders may be classified into two groups, language-based type learning disorders including reading and writing disorder, and nonverbal type learning disorder (NLD) such as those relating to mathematics & visuospatial skills, and those in the autism spectrum. Converging evidence indicates that reading disorder represents a disorder within the language system and more specifically within a particular subcomponent of that system, phonological processing. Recent advances in neuroimaging technology, particularly the development of fMRI, provide evidences of a neurobiological basis for reading disorder, specifically a disruption of two left hemisphere posterior brain systems, one parieto-temporal, the other occipito-temporal. The former is the reading system for beginner reading, the latter for skilled reading. Compensatory engagement of anterior systems around the inferior frontal gyrus(Broca's area) and a posterior(right occipito-temporal) system is noted in persistent poor readers in long-term follow up study. The theoretical model proposed to explain NLD's source is not right hemisphere damage, but rather the white matter model. The working hypothesis of the white matter model is that the underdevelopment of, damage to, or dysfunction of cerebral white matter(long myelinated fibers) is the source of this disorder. The role of an evidence-based effective intervention in the remediation of children with learning disorder is discussed.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
• /
• v.28 no.1
• /
• pp.4-13
• /
• 2017

The seeds of addiction are typically sown years prior to the onset of addictive substance use or engagement in addictive behaviors, due to the priming of the reward pathway (RewP) by alterations in the mechanism of stress-signaling from the hypothalamic-pituitary-adrenal axis (HPA) and related pathways. Excessive stress from a single-event and/or cumulative life experiences during childhood, such as those documented in the Adverse Childhood Experiences Study, is translated into neurobiological toxicity that alters the set-point of the HPA axis and limbic system homeostasis [suggested new term: regulation pathway (RegP)]. The resultant alteration of the RegP not only increases the risk for psychiatric and physical illness, but also that for early onset and chronic addictions by dysregulating the RewP. This paper reviews the interface of these symbiotic pathways that result in the phenotypic pathology of emotional dysregulation, cognitive impairment, and compulsive behaviors, as well as morbidity and shorter life expectancy when dysregulated by chronic stress.

• Journal of the Korean Applied Science and Technology
• /
• v.37 no.4
• /
• pp.762-768
• /
• 2020

This study aimed to investigate the effect of ladder-climbing exercise training on neurobiological markers in the hippocampus of mice with type 2 diabetes (T2DM). Twenty-one C57BL/6 male mice were randomly assigned to the non-diabetic control (NDC, n = 7), diabetic control (DC, n = 7), and diabetic training (DT, n = 7) groups. The DT group performed ladder-climbing training (LCT) five times a week for eight weeks. We measured the levels of hippocampal neurobiological markers (catalase [CAT], brain-derived neurotrophic factor [BDNF], nerve growth factor [NGF], amyloid-beta [Aβ], tau, and CC motif chemokine ligand 11 [CCL11]). The BDNF levels were significantly higher in the DT group than in the DC group (p < 0.05). The Aβ and CCL11 levels were significantly higher in the DC group than in the NDC and DT groups (p < 0.05). The tau levels were significantly higher in the DC group than in the NDC group (p < 0.05). However, there was no significant difference in CAT and NGF levels among the groups (p > 0.05). These results suggest that while T2DM could induce neurodegeneration, LCT may be effective in alleviating neurodegeneration caused by T2DM.

• Korean Journal of Acupuncture
• /
• v.38 no.2
• /
• pp.75-99
• /
• 2021

Objectives : The purpose of this study is to analyze animal behavioral changes and related neurobiological mechanisms in recent studies using animal models with pain and depression. Methods : We conducted database search in Pubmed, NDSL, and EMBASE up to January 2021. Included studies were classified as depression-like behavior observed in pain model, pain-like behavior observed in depression model, and pain and depression comorbidity model. The results of pain- and depression-like behaviors, the changes of neurobiological mechanisms, and the treatment methods such as drugs, natural substance-derived chemicals, or acupuncture were analyzed. Results : We included 124 studies (81 studies in depression-like behavior observed in pain model, 19 studies in pain-like behavior observed in depression model, and 24 studies in pain and depression comorbidity model). Pain and depression comorbidity animal models were induced using various methods by drugs or surgery. Von frey test, a method for evaluating mechanical allodynia was the most commonly used for measuring pain-like behavior and the forced swimming test was the most commonly used for measuring depression-likes behavior. The changes of neurobiological factors, such as decrease of 5-hydroxytryptamine and increase of oxidative stress and pro-inflammation cytokines were generally changed in the frontal cortex, hippocampus, thalamus, and spinal cord in all types of models. For treating pain and depression-like behaviors, various types of drugs such as antidepressant, tranquilizer, analgesic, and natural substance-derived chemicals were used. Acupuncture treatment was used in 4 studies. Conclusions : In the future, more diverse studies on the combined model of pain and depression need to be conducted. In addition, it is necessary to establish a mechanistic basis for the development of various treatments by identifying the common mechanisms of pain and depression.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
• /
• v.16 no.2
• /
• pp.173-182
• /
• 2005

This review is a clinical and research update of recent literature related to childhood onset schizophrenia (with an onset of psychosis by age 12). Childhood onset schizophrenia(COS) is a rare disorder, but that may represent a more homogeneous patient population in which to search for risk or etiologic factors of schizophrenia. These overview data show that COS shares the same clinical and neurobiological features as later onset forms of the disorder. Compared with later onset schizophrenia, however, this subgroup of patients appear to have more severe premorbid neurodevelopmental abnormalities, more cytogenic abnormalies, poor outcome, and potentially greater family histories of schizophrenia and associated spectrum disorders. Future studies of this subgroup may provide important clues as to the genetic basis for schizophrenia and how gene products influence certain feature of the disease, such as age of onset and mode of inheritance.

• Korean Journal of Biological Psychiatry
• /
• v.4 no.2
• /
• pp.188-193
• /
• 1997

Along with psychosocial factors of suicide, biological backgrounds of suicide are explored by extensive works mostly on biological markers, neurobiological models, genetic bases, and relationships with aggression and violence. The biology of suicide confers on neurotransmitters in central nervous system exploring metabolites, receptor binding affinities, neuroendocrine challenge tests in brain, cerebrospinal fluid, blood and etc. The major concerns with suicide are focused mainly on serotonin system : low CSF 5-HIAA concentration, higher $5-HT_2$ receptor binding, and blunt prolactin response to fenfluramine. Postmortem study, in vivo study, genetic contributions, and some other issues such as suicidal methods, serum cholesterol, alcohol, and selective serotonin reuptake inhibitors are reviewed and discussed.

• The Journal of Korea Robotics Society
• /
• v.17 no.1
• /
• pp.86-92
• /
• 2022

Utilization of small robots in psychology and biology provides a new breakthrough in understanding the neurobiological mechanisms of various animal behavior. The expansion of robot use in animal research is partly due to increased availability of economically plausible mobile robots and also due to the current shift in animal research toward more ecologically valid experiments. Ground-breaking experimental findings are expected when the behavioral variables are manipulated in more natural situations. In addition, the results from laboratory could be generalized more easily with added ecological validity. The current paper attempts to review a wide range of applications of animal robots used to study animal behavior and to highlight major advantages and limitations. In particular, this review focuses more on the psychological impact of animal robots than engineering details about their structure and operation. Finally, this review will provide some practical considerations when employing robots in animal experiments.

• Dementia and Neurocognitive Disorders
• /
• v.22 no.1
• /
• pp.16-27
• /
• 2023

Alzheimer's disease (AD), one of the most representative neurodegenerative diseases, has diverse neurobiological and pathophysiological mechanisms. Treatment strategies targeting a single mechanism have repeated faced failures because the mechanism of neuronal cell death is very complex that is not fully understood yet. Since complex mechanisms exist to explain AD, a variety of diagnostic biomarkers for diagnosing AD are required. Moreover, standardized evaluations for comprehensive diagnosis using neuropsychological, imaging, and laboratory tools are needed. In this review, we summarize the latest clinical, neuropsychological, imaging, and laboratory evaluations to diagnose patients with AD based on our own experience in conducting a prospective study.

• Biomolecules & Therapeutics
• /
• v.22 no.5
• /
• pp.406-413
• /
• 2014

to valproic acid (VPA) during pregnancy produces ASD-like core behavioral phenotypes as well as hyperactivity in offspring both in human and experimental animals, which makes it a plausible model to study ASD-related neurobiological processes. In this study, we examined the effects of two of currently available attention defecit hyperactivity disorder (ADHD) medications, methylphenidate (MPH) and atomoxetine (ATX) targeting dopamine and norepinephrine transporters (DAT and NET), respectively, on hyperactive behavior of prenatally VPA-exposed rat offspring. In the prefrontal cortex of VPA exposed rat offspring, both mRNA and protein expression of DAT was increased as compared with control. VPA function as a histone deacetylase inhibitor (HDACi) and chromatin immunoprecipitation experiments demonstrated that the acetylation of histone bound to DAT gene promoter was increased in VPA-exposed rat offspring suggesting epigenetic mechanism of DAT regulation. Similarly, the expression of NET was increased, possibly via increased histone acetylation in prefrontal cortex of VPA-exposed rat offspring. When we treated the VPA-exposed rat offspring with ATX, a NET selective inhibitor, hyperactivity was reversed to control level. In contrast, MPH that inhibits both DAT and NET, did not produce inhibitory effects against hyperactivity. The results suggest that NET abnormalities may underlie the hyperactive phenotype in VPA animal model of ASD. Profiling the pharmacological responsiveness as well as investigating underlying mechanism in multiple models of ASD and ADHD may provide more insights into the neurobiological correlates regulating the behavioral abnormalities.