• The Journal of Korea Robotics Society
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• v.1 no.2
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• pp.163-171
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• 2006

This paper introduces the research progress on the artificial brain in the Telerobotics and Control Laboratory at KAIST. This series of studies is based on the assumption that it will be possible to develop an artificial intelligence by copying the mechanisms of the animal brain. Two important brain mechanisms are considered: spike-timing dependent plasticity and dopaminergic plasticity. Each mechanism is implemented in two coding paradigms: spike-codes and rate-codes. Spike-timing dependent plasticity is essential for self-organization in the brain. Dopamine neurons deliver reward signals and modify the synaptic efficacies in order to maximize the predicted reward. This paper addresses how artificial intelligence can emerge by the synergy between self-organization and reinforcement learning. For implementation issues, the rate codes of the brain mechanisms are developed to calculate the neuron dynamics efficiently.

• Biomolecules & Therapeutics
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• v.20 no.4
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• pp.357-370
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• 2012

Radiation therapy, the most commonly used for the treatment of brain tumors, has been shown to be of major significance in tumor control and survival rate of brain tumor patients. About 200,000 patients with brain tumor are treated with either partial large field or whole brain radiation every year in the United States. The use of radiation therapy for treatment of brain tumors, however, may lead to devastating functional deficits in brain several months to years after treatment. In particular, whole brain radiation therapy results in a significant reduction in learning and memory in brain tumor patients as long-term consequences of treatment. Although a number of in vitro and in vivo studies have demonstrated the pathogenesis of radiation-mediated brain injury, the cellular and molecular mechanisms by which radiation induces damage to normal tissue in brain remain largely unknown. Therefore, this review focuses on the pathophysiological mechanisms of whole brain radiation-induced cognitive impairment and the identification of novel therapeutic targets. Specifically, we review the current knowledge about the effects of whole brain radiation on pro-oxidative and pro-inflammatory pathways, matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinases (TIMPs) system and extracellular matrix (ECM), and physiological angiogenesis in brain. These studies may provide a foundation for defining a new cellular and molecular basis related to the etiology of cognitive impairment that occurs among patients in response to whole brain radiation therapy. It may also lead to new opportunities for therapeutic interventions for brain tumor patients who are undergoing whole brain radiation therapy.

• The Journal of Korean Physical Therapy
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• v.13 no.3
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• pp.791-797
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• 2001

After brain injury, patients show a wide range in the degree of recovery. By a variety of mechanisms, the human brain is constantly undergoing plastic changes. Spontaneous recovery from brain injury in the chronic stage omes about because of plasticity. The brain regions are altered. resulting in functionally modified cortical network. This review cnsidered the neural plasticity from cellular and molecular mechanisms of synapse formation to behavioural recovery from brain injury in elderly humans. The stimuli required to elicit plasticity are thought to be activity-dependent elements. especially exercise and learning. Knowledge about the physiology of brain plasticity has led to the development of methods for rehabilitation.

• Korean Journal of Biological Psychiatry
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• v.30 no.1
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• pp.1-6
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• 2023

Many psychiatric disorders are associated with brain functional dysfunctions and neuronal degeneration. According to the research so far, enhanced brain plasticity reduces neurodegeneration and recovers neuronal damage. Brain-derived neurotrophic factor (BDNF) is one of the most extensively studied neurotrophins in the mammalian brain that plays major roles in neuronal survival, development, growth, and maintenance of neurons in brain circuits related to emotion and cognitive function. Also, BDNF plays an important role in brain plasticity, influencing dendritic spines in the hippocampus neurogenesis. Changes in neurogenesis and dendritic density can improve psychiatric symptoms and cognitive functions. BDNF has potent effects on brain plasticity through biochemical mechanisms, cellular signal pathways, and epigenetic changes. There are pharmacological and non-pharmacological interventions to increase the expression of BDNF and enhance brain plasticity. Non-pharmacological interventions such as physical exercise, nutritional change, environmental enrichment, and neuromodulation have biological mechanisms that increase the expression of BDNF and brain plasticity. Non-pharmacological interventions are cost-effective and safe ways to improve psychiatric symptoms.

• BMB Reports
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• v.49 no.9
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• pp.474-487
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• 2016

Itch is one of the most distressing sensations that substantially impair quality of life. It is a cardinal symptom of many skin diseases and is also caused by a variety of systemic disorders. Unfortunately, currently available itch medications are ineffective in many chronic itch conditions, and they often cause undesirable side effects. To develop novel therapeutic strategies, it is essential to identify primary afferent neurons that selectively respond to itch mediators as well as the central nervous system components that process the sensation of itch and initiate behavioral responses. This review summarizes recent progress in the study of itch, focusing on itch-selective receptors, signaling molecules, neuronal pathways from the primary sensory neurons to the brain, and potential decoding mechanisms based on which itch is distinguished from pain.

• Molecules and Cells
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• v.41 no.5
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• pp.373-380
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• 2018

Synapses and neural circuits form with exquisite specificity during brain development to allow the precise and appropriate flow of neural information. Although this property of synapses and neural circuits has been extensively investigated for more than a century, molecular mechanisms underlying this property are only recently being unveiled. Recent studies highlight several classes of cell-surface proteins as organizing hubs in building structural and functional architectures of specific synapses and neural circuits. In the present minireview, we discuss recent findings on various synapse organizers that confer the distinct properties of specific synapse types and neural circuit architectures in mammalian brains, with a particular focus on the hippocampus and cerebellum.

• Molecules and Cells
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• v.47 no.1
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• pp.100005.1-100005.15
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• 2024

Amyotrophic lateral sclerosis is a devastating neurodegenerative disease with a complex genetic basis, presenting both in familial and sporadic forms. The hexanucleotide (G₄C₂) repeat expansion in the C9orf72 gene, which triggers distinct pathogenic mechanisms, has been identified as a major contributor to familial and sporadic Amyotrophic lateral sclerosis cases. Animal models have proven pivotal in understanding these mechanisms; however, discrepancies between models due to variable transgene sequence, expression levels, and toxicity profiles complicate the translation of findings. Herein, we provide a systematic comparison of 7 publicly available Drosophila transgenes modeling the G₄C₂ expansion under uniform conditions, evaluating variations in their toxicity profiles. Further, we tested 3 previously characterized disease-modifying drugs in selected lines to uncover discrepancies among the tested strains. Our study not only deepens our understanding of the C9orf72 G₄C₂ mutations but also presents a framework for comparing constructs with minute structural differences. This work may be used to inform experimental designs to better model disease mechanisms and help guide the development of targeted interventions for neurodegenerative diseases, thus bridging the gap between model-based research and therapeutic application.

• Korean Journal of Biological Psychiatry
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• v.28 no.2
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• pp.23-35
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• 2021

Fear conditioning and extinction, which are adaptive processes to learn and avoid potential threats, have essential roles in the pathophysiology of anxiety disorders. Experimental fear conditioning and extinction have been used to identify the mechanism of fear and anxiety in humans. However, the brain-based mechanisms of fear conditioning and extinction are yet to be established. In the current review, we summarized the results of neuroimaging studies that examined the brain changes-functional activity and structures-regarding fear conditioning or extinction in healthy individuals. The functional activity of the amygdala, insula, anterior cingulate gyrus, ventromedial prefrontal cortex, and hippocampus changed dynamically with both fear conditioning and extinction. This review may provide an up-to-date summary that may broaden our understanding of pathophysiological mechanisms of anxiety disorder. In addition, the brain regions that are involved in the fear conditioning and extinction may be considered as potential treatment targets in the future studies.

• Korean Journal of Exercise Nutrition
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• v.23 no.4
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• pp.23-25
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• 2019

Recent research suggests that the brain has capable of remarkable plasticity and physical activity can enhance it. In this editorial letter, we summarize the role of hippocampal plasticity in brain functions. Furthermore, we briefly sketched the factors and mechanisms of motion that influence brain plasticity. We conclude that physical activity can be an encouraging intervention for brain restoration through neuronal plasticity. At the same time, we suggest that a mechanistic understanding of the beneficial effects of exercise should be accompanied in future studies.

• Proceedings of the Korean Society of Toxicology Conference
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• 2006.11a
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• pp.55-64
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• 2006

The fetal central nervous system (CNS) is sensitive to diverse environmental factors, such as alcohol, heavy metals, irradiation, mycotoxins, neurotransmitters, and DNA damage, because a large number of processes occur during an extended period of development. Fetal neural damage is an important issue affecting the completion of normal CNS development. As many concepts about the brain development have been recently revealed, it is necessary to compare the mechanism of developmental abnormalities induced by extrinsic factors with the normal brain development. To clarify the mechanism of fetal CNS damage, we used one experimental model in which 5-azacytidine (5AZC), a DNA damaging and demethylating agent, was injected to the dams of rodents to damage the fetal brain. 5AzC induced cell death (apoptosis)and cell cycle arrest in the fetal brain, and it lead to microencephaly in the neonatal brain. We investigated the mechanism of apoptosis and cell cycle arrest in the neural progenitor cells in detail, and demonstrated that various cell cycle regulators were changed in response to DNA damage. p53, the guardian of genome, played a main role in these processes. Further, using DNA microarray analysis, tile signal cascades of cell cycle regulation were clearly shown. Our results indicate that neural progenitor cells have the potential to repair the DNA damages via cell cyclearrest and to exclude highly affected cells through the apoptotic process. If the stimulus and subsequent DNA damage are high, brain development proceeds abnormally and results in malformation in the neonatal brain. Although the mechanisms of fetal brain injury and features of brain malformation afterbirth have been well studied, the process between those stages is largely unknown. We hypothesized that the fetal CNS has the ability to repair itself post-injuring, and investigated the repair process after 5AZC-induced damage. Wefound that the damages were repaired by 60 h after the treatment and developmental processes continued. During the repair process, amoeboid microglial cells infiltrated in the brain tissue, some of which ingested apoptotic cells. The expressions of genes categorized to glial cells, inflammation, extracellular matrix, glycolysis, and neurogenesis were upregulated in the DNA microarray analysis. We show here that the developing brain has a capacity to repair the damage induced by the extrinsic stresses, including changing the expression of numerous genes and the induction of microglia to aid the repair process.