• Proceedings of the PSK Conference
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• 2003.04a
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• pp.232.2-232.2
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• 2003

Many neurodegenerative disorders such as stroke, Alzheimer's disease, and Parkinson's disease have been known to be associated with an excessive generation of reactive oxygen species (ROS) and oxidative stress. Therefore, the antioxidants have recently received much attention as therapeutic agent for the treatment of neurodegenerative disease. (omitted)

• BMB Reports
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• v.55 no.12
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• pp.621-626
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• 2022

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease characterized by the degeneration of motor neurons in the spinal cord. Main symptoms are manifested as weakness, muscle loss, and muscle atrophy. Some studies have reported that alterations in sphingolipid metabolism may be intimately related to neurodegenerative diseases, including ALS. Acid sphingomyelinase (ASM), a sphingolipid-metabolizing enzyme, is considered an important mediator of neurodegenerative diseases. Herein, we show that ASM activity increases in samples from patients with ALS and in a mouse model. Moreover, genetic inhibition of ASM improves motor function impairment and spinal neuronal loss in an ALS mouse model. Therefore, these results suggest the role of ASM as a potentially effective target and ASM inhibition may be a possible therapeutic approach for ALS.

• Journal of Ginseng Research
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• v.36 no.4
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• pp.342-353
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• 2012

Ginseng, the root of the Panax ginseng, has been a popular and widely-used traditional herbal medicine in Korea, China, and Japan for thousands of years. Now it has become popular as a functional health food and is used globally as a natural medicine. Evidence is accumulating in the literature on the physiological and pharmacological effects of P. ginseng on neurodegenerative diseases. Possible ginseng- or ginsenosides-mediated neuroprotective mechanisms mainly involve maintaining homeostasis, and anti-inflammatory, anti-oxidant, anti-apoptotic, and immune-stimulatory activities. This review considers publications dealing with the various actions of P. ginseng that are indicative of possible neurotherapeutic efficacies in neurodegenerative diseases and neurological disorders such as Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis and multiple sclerosis.

• The Journal of Internal Korean Medicine
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• v.41 no.6
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• pp.993-1014
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• 2020

Objective: Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. Antioxidant stress and inflammatory reactions are important causes of neurodegenerative diseases and are major causes of PD. Many animal experiments have been aimed at treating PD using the antioxidant effects of various traditional medicines and dietary supplements. This review reports the research investigating the antioxidant effects of herbs in in vivo PD models. Methods: The study consisted of a database search for articles related to PD and herbal treatments using the OASIS, NDSL, KTKP, Korean KISS, PubMed, Science Direct, CNKI, Wanfang, and J-STAGE databases. The search period was limited from the start of the search engine application to November 14, 2019. Studies were selected to confirm the antioxidant effects of herbal medicines in an in vivo PD model. Results: Eighty-two studies were summarized for plant species, extracts (or compounds), animal models, neurotoxins, and functional results. The most frequently used herbal materials were Bacopa monnieri, Camellia sinensis, Centella asiatica, and Withania somnifera. MPTP and 6-OHDA were the most commonly used neurotoxins for inducing PD. Most studies confirmed an increased expression and activation of antioxidant enzymes and a decrease in oxidative stress. Herbal materials showed their antioxidant effects regardless of the order of treatment and confirmed their possible use as treatments for the prevention and treatment of neurodegeneration. Conclusion: Many herbal medicines have antioxidant effects and are likely to be effective in delaying neurodegenerative damage by inhibiting or reducing oxidative stress by expression of antioxidant enzymes.

• BMB Reports
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• v.50 no.1
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• pp.5-11
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• 2017

One of the characteristics of the neurons that distinguishes them from other cells is their complex and polarized structure consisting of dendrites, cell body, and axon. The complexity and diversity of dendrites are particularly well recognized, and accumulating evidences suggest that the alterations in the dendrite structure are associated with many neurodegenerative diseases. Given the importance of the proper dendritic structures for neuronal functions, the dendrite pathology appears to have crucial contribution to the pathogenesis of neurodegenerative diseases. Nonetheless, the cellular and molecular basis of dendritic changes in the neurodegenerative diseases remains largely elusive. Previous studies in normal condition have revealed that several cellular components, such as local cytoskeletal structures and organelles located locally in dendrites, play crucial roles in dendrite growth. By reviewing what has been unveiled to date regarding dendrite growth in terms of these local cellular components, we aim to provide an insight to categorize the potential cellular basis that can be applied to the dendrite pathology manifested in many neurodegenerative diseases.

• Nuclear Medicine and Molecular Imaging
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• v.42 no.sup1
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• pp.166-171
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• 2008

PET of the cerebral metabolic rate of glucose is increasingly used to support the clinical diagnosis in the examination of patients with suspected major neurodegenerative disorders, such as Alzheimer's disease. $^{18}F-FDG$ PET has been reported to have high diagnostic performance, especially, very high sensitivity in the diagnosis and clinical assessment of therapeutic efficacy. According to clinical research data hitherto, $^{18}F-FDG$ PET is expected to be an effective diagnostic tool in early and differential diagnosis of Alzheimer's disease. Since 2004, Medicare covers $^{18}F-FDG$ PET scans for the differential diagnosis of fronto-temporal dementia (FTD) and Alzheimer's disease (AD) under specific requirements; or, its use in a CMS approved practical clinical trial focused on the utility of $^{18}F-FDG$ PET in the diagnosis or treatment of dementing neurodegenerative diseases.

• BMB Reports
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• v.50 no.5
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• pp.237-246
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• 2017

Synapse is the basic structural and functional component for neural communication in the brain. The presynaptic terminal is the structural and functionally essential area that initiates communication and maintains the continuous functional neural information flow. It contains synaptic vesicles (SV) filled with neurotransmitters, an active zone for release, and numerous proteins for SV fusion and retrieval. The structural and functional synaptic plasticity is a representative characteristic; however, it is highly vulnerable to various pathological conditions. In fact, synaptic alteration is thought to be central to neural disease processes. In particular, the alteration of the structural and functional phenotype of the presynaptic terminal is a highly significant evidence for neural diseases. In this review, we specifically describe structural and functional alteration of nerve terminals in several neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD).

• 대한약리학회:학술대회논문집
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• 2006.10a
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• pp.107.2-107.2
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• 2006

• Biomolecules & Therapeutics
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• v.20 no.2
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• pp.133-143
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• 2012

Matrix metalloproteinases (MMPs) are a subfamily of zinc-dependent proteases that are re-sponsible for degradation and remodeling of extracellular matrix proteins. The activity of MMPs is tightly regulated at several levels including cleavage of prodomain, allosteric activation, com-partmentalization and complex formation with tissue inhibitor of metalloproteinases (TIMPs). In the central nervous system (CNS), MMPs play a wide variety of roles ranging from brain devel-opment, synaptic plasticity and repair after injury to the pathogenesis of various brain disorders. Following general discussion on the domain structure and the regulation of activity of MMPs, we emphasize their implication in various brain disorder conditions such as Alzheimer's disease, multiple sclerosis, ischemia/reperfusion and Parkinson's disease. We further highlight accumu-lating evidence that MMPs might be the culprit in Parkinson's disease (PD). Among them, MMP-3 appears to be involved in a range of pathogenesis processes in PD including neuroinflamma-tion, apoptosis and degradation of ${\alpha}$-synuclein and DJ-1. MMP inhibitors could represent poten-tial novel therapeutic strategies for treatments of neurodegenerative diseases.

• Journal of Microbiology and Biotechnology
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• v.23 no.3
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• pp.279-288
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• 2013

Phosphorylation and dephosphorylation of proteins trigger many critical events involved in cellular response, such as regulation of enzymatic activity, protein conformational change, protein-protein interaction, and cellular localization. Any malfunction of protein phosphorylation leads to a diseased state such as diabetes, cancer, and even neurodegenerative diseases. In order to comprehend the molecular view of the complex biological processes of these diseases in depth, very sensitive and detailed analytical methods are necessary for identification of the phosphorylated residues in a protein. As part of these efforts, phosphoproteomics has been developed and applied for the elucidation of neurodegenerative diseases. In this review, we present a brief summary of phosphoproteomics approaches that are now routinely used in biomedical research, and describe the biomedical application of phosphoproteomics especially in Alzheimer's and other neurodegenerative diseases.