• BMB Reports
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• v.52 no.12
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• pp.679-688
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• 2019

The decrease of metabolism in the brain has been observed as the important lesions of Alzheimer's disease (AD) from the early stages of diagnosis. The cumulative evidence has reported that the failure of mitochondria, an organelle involved in diverse biological processes as well as energy production, maybe the cause or effect of the pathogenesis of AD. Both amyloid and tau pathologies have an impact upon mitochondria through physical interaction or indirect signaling pathways, resulting in the disruption of mitochondrial function and dynamics which can trigger AD. In addition, mitochondria are involved in different biological processes depending on the specific functions of each cell type in the brain. Thus, it is necessary to understand mitochondrial dysfunction as part of the pathological phenotypes of AD according to each cell type. In this review, we summarize that 1) the effects of AD pathology inducing mitochondrial dysfunction and 2) the contribution of mitochondrial dysfunction in each cell type to AD pathogenesis.

• YAKHAK HOEJI
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• v.54 no.5
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• pp.323-327
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• 2010

Translationally controlled tumor protein (TCTP) activates basophils to release histamine and causes chronic inflammation. It was also reported that TCTP significantly reduced in brain of Alzheimer's Disease and Down Syndrome as compared to normal person, suggesting that TCTP might be involved in cognitive function. We wondered whether TCTP could act as a general inducer in neurotransmitters release in brain. We, therefore, investigated the role of TCTP in PC12 cell line which expressed neuronal properties. We found that TCTP could activate JNK, and the activity was inhibited by pretreatment of dicoumarol, a JNK inhibitor. However, TCTP could not activate ERK that has known to be involved in neurotransmitter release. These suggest TCTP did not participate in neurotransmitter release from PC12 cells, and TCTP might not be a general inducer in neurotransmitter release.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.5
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• pp.223-229
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• 2006

The emerging concept of the 'neurovascular unit' may enable a powerful paradigm shift for neuroscience. Instead of a pure focus on the 'neurobiology' of disease, an opportunity now exists to return to a more integrative approach. The neurovascular unit emphasizes that signaling between vascular and neuronal compartments comprise the basis for both function and dysfunction in brain. Hence, brain disorders are not just due to death of neurons, but instead manifested as cell signaling perturbations at the neurovascular interface. In this mini-review, we will examine 3 examples of this hypothesis: neurovascular mechanisms involved in the thrombolytic therapy of stroke, the crosstalk between neurogenesis and angiogenesis, and the link between vascular dysfunction and amyloid pathology in Alzheimer's disease. An understanding of cell-cell and cell-matrix signaling at the neurovascular interface may yield new approaches for targeting CNS disorders.

• The Korean Journal of Nuclear Medicine
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• v.37 no.1
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• pp.13-23
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• 2003

Neurodegenerative disorders cause a variety of dementia including Alzheimer disease, frontotemporal dementia, dementia with Lewy bodies, corticobasal degeneration, progressive supranuclear palsy, and Huntington's disease. PET scan is useful for early detection and differential diagnosis of these dementing disorders. Also, it provides valuable information about clinico-anatomical correlation, allowing better understanding of function of brain. Here we discuss recent achievements PET studies regarding these dementing disorders. Future progress in PET technology, new tracers, and image analysis will play an important role in further clarifying the disease pathophysiology and brain functions.

• Biomedical Science Letters
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• v.25 no.2
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• pp.113-122
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• 2019

Long-non coding RNAs (LncRNAs) constitute a wide and extremely diverse family of RNA transcripts that are greater than 200 base pairs in length and are not translated into proteins. X-inactive specific transcript (XIST) was the first long non-coding RNA to be discovered, back in 1991. Its function in X-chromosome inactivation has been extensively studied for three decades, though other functional roles of XIST that involve a variety of fascinating mechanisms remain to be elucidated. Here, we review the emerging oncogenic role of XIST in various human cancers.

• Therapeutic Science for Rehabilitation
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• v.6 no.2
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• pp.37-45
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• 2017

Background: The presence of visuospatial impairment can make patients slow functional recovery and impede the rehabilitation process in TBI patients. Objective: The aim of this study is to investigate effects of prism adaptation treatment for functional outcomes in patients following traumatic brain injury. Methods: The subject received prism adaptation treatment for 2 weeks additionally during traditional rehabilitation for 4 weeks. The Patient has prism adaptation treatment while wearing wedge prisms that shift the external environment about $12^{\circ}$ leftward. The patient received 10 sessions, 15-20min each session. Outcome measures were visuospatial deficit(line bisection, latter cancellation), Visual and spatial perception(LOTCA-visual perception and spatial perception), motor function of upper extremity(FMA U/E; Fugl-Meyer motor assessment upper extremity, ARAT; Action research arm test), balance(BBS; Berg Balance Scale), mobility(FAC; Functional ambulation classification) and functional level(FIM; Functional independent measure). All Assessments took place on study entry and post-treatment assessments were performed at discharge from the hospital. Results: After prism adaptation, the visuospatial impairment scores improved as indicated in the line bisection(-15.2 to -6.02), latter cancellation(2 to 0) and LOTCA- spatial perception scores(7 to 9). The upper motor function improved as indicated in the scores of affected FMA U/E(21 to 40) and ARAT(4 to 22). Ambulation and balance improved as indicated in the BBS scores(25 to 38) and FAC scores(0 to 4). ADL function improved as indicated in the FIM total scores 54 to 70(motor 34 to 61, cognition 20 to 29). Conclusion: Prism adaptation did improve functional level such as motor functions and ADL abilities in TBI patient. Further research is recommended.

• Annals of Clinical Neurophysiology
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• v.9 no.1
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• pp.5-10
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• 2007

Background: Bell's palsy (BP) is a self-limited rapid onset facial palsy that is non-life-threatening and has a generally favorable prognosis. Facial paralysis can be caused by numerous conditions, all of which should be excluded before the diagnosis of BP is reached. The etiopathogenesis and clinical course of BP are uncertain. So we analyzed the epidemiology and clinical course of BP patients. Methods: The subjects include 100 cases of BP examined during the period of 18 months. Careful clinical history, neurologic examinations, laboratory tests, electrophysiologic studies, and brain imaging were performed. Follow-up examinations were done once a week during the first month and subsequently once a month until normal function was restored or for up to 3 months. Facial nerve function was assessed by House-Brackman (HB) facial nerve grading scale and electrophysiologic studies. Results: Except 13 recurrent BP patients, we analyzed 87 BP patients. Forty-four (50.6%) were men and 43(49.4%) were women and the mean age was 51.0(${\pm}16.6$) years. Three (3.4%) patients showed a familial tendency. The initial examination within 1 week after attack revealed 35.2% was below HB grade 4 and 64.8% was above grade 3. The associated symptoms are as follows; postauricular pain, increase tear flow, taste change, hyperacusis and drooling. The initial facial nerve conduction study and blink reflex within 1 week after attack showed abnormal findings in 12.6% and 100%, respectively. Brain MRI was performed in 59(67.8%) patients and showed abnormal enhancement of affected nerve in 57(96.6%). Follow-up examination showed that 78.2% of the patients partially improved within 4 weeks and completely improved within 3 months. Finally 80.5% of the total patients obtained normal function in 3 months. Conclusions: We report epidemiologic, clinical, electrophysiologic and radiologic characteristics of BP patients.

• The Journal of Korean Physical Therapy
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• v.31 no.2
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• pp.67-75
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• 2019

Purpose: Patients with brain damage suffer from limitations in performing the activities of daily living (ADL) because of their motor function and visual perception impairment. The aim of this study was to help improve the motor function and visual perception ability of patients with brain damage by providing them with virtual reality-based contents. The usability results of the patients and specialists group were also evaluated. Methods: The ADL contents consisted of living room, kitchen, veranda, and convenience store, similar to a real home environment, and these were organized by a rehabilitation specialist (e.g., neurologist, physiotherapist, and occupational therapist). The contents consisted of tasks, such as turning on the living room lights, organizing the drawers, organizing the kitchen, watering the plants on the veranda, and buying products at convenience stores. To evaluate the usability of the virtual reality-based visual cognitive rehabilitation service, general elderly subjects (n=11), stroke patients (n=7), stroke patients with visual impairment (n=4), and rehabilitation specialists (n=11) were selected. The questionnaires were distributed to the subjects who were using the service, and the subjective satisfaction of individual users was obtained as data. The data were analyzed using SPSS 21.0 software. The general characteristics of the users and the evaluation scores of the experts were analyzed using descriptive statistics. Results: The usability test result of this study showed that the mean value of the questionnaire related to content understanding and difficulty was high, between 4-5 points. Conclusion: The virtual reality rehabilitation service of this study is an efficient service that can improve the function, interest, and motivation of stroke patients.

• The Korea Journal of Herbology
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• v.30 no.2
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• pp.43-48
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• 2015

Objectives : The aim of this study was to investigate the memory enhancing properties of extract of Hoelen Cum Radix (HCR) and its possible mechanism in mice of normal condition. Methods : We evaluated the effects of HCR on cognitive function and memory enhancement in normal mice. Male ICR mice were orally administrated with HCR 100 mg/kg for 7 days and equal volume of saline was administrated to the control group in the same condition. We conducted two behavioral tests which measure the spatial working memory (Y-maze test) and cognitive fear memory (passive avoidance test). We also investigated whether HCR affects the hippocampal neurogenesis in the brain. To assess the effects of HCR on neural progenitor cell differentiation and neurite outgrowth in the early stage of hippocampal neurogenesis, we performed doublecortin (DCX), a direct neurogenesis marker, immunohistochemical analysis in the dentate gyrus (DG) of the mouse hippocampus. Results : HCR significantly enhanced memory and cognitive function as determined by the Y-maze test (p<0.05) and passive avoidance test (p<0.001). Moreover, HCR increased DCX positive cells (p<0.01) and neurite length (p<0.01) compared to the control group. These results indicated that HCR stimulates differentiation of neural progenitor cells and promotes neurite outgrowth in hippocampal DG of the mice. Conclusion : We concluded that HCR shows memory enhancing effects through the stimulation of hippocampal neurogenesis as a consequence of accelerated neuronal differentiation and neurite outgrowth in the DG of the hippocampus after HCR treatment.

• The Korean Journal of Pain
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• v.36 no.1
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• pp.72-83
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• 2023

Background: Globally, spinal cord injury (SCI) results in a big burden, including 90% suffering permanent disability, and 60%-69% experiencing neuropathic pain. The main causes are oxidative stress, inflammation, and degeneration. The efficacy of the stem cell secretome is promising, but the role of human neural stem cell (HNSC)-secretome in neuropathic pain is unclear. This study evaluated how the mechanism of HNSC-secretome improves neuropathic pain and locomotor function in SCI rat models through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities. Methods: A proper experimental study investigated 15 Rattus norvegicus divided into normal, control, and treatment groups (30 µL HNSC-secretome, intrathecal in the level of T10, three days post-traumatic SCI). Twenty-eight days post-injury, specimens were collected, and matrix metalloproteinase (MMP)-9, F2-Isoprostanes, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, and brain derived neurotrophic factor (BDNF) were analyzed. Locomotor recovery was evaluated via Basso, Beattie, and Bresnahan scores. Neuropathic pain was evaluated using the Rat Grimace Scale. Results: The HNSC-secretome could improve locomotor recovery and neuropathic pain, decrease F2-Isoprostane (antioxidant), decrease MMP-9 and TNF-α (anti-inflammatory), as well as modulate TGF-β and BDNF (neurotrophic factor). Moreover, HNSC-secretomes maintain the extracellular matrix of SCI by reducing the matrix degradation effect of MMP-9 and increasing the collagen formation effect of TGF-β as a resistor of glial scar formation. Conclusions: The present study demonstrated the mechanism of HNSC-secretome in improving neuropathic pain and locomotor function in SCI through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities.