• BMB Reports
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• 제53권1호
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• pp.28-34
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• 2020

Sphingolipids are ubiquitous building blocks of eukaryotic cell membranes that function as signaling molecules for regulating a diverse range of cellular processes, including cell proliferation, growth, survival, immune-cell trafficking, vascular and epithelial integrity, and inflammation. Recently, several studies have highlighted the pivotal role of sphingolipids in neuroinflammatory regulation. Sphingolipids have multiple functions, including induction of the expression of various inflammatory mediators and regulation of neuroinflammation by directly effecting the cells of the central nervous system. Accumulating evidence points to sphingolipid engagement in neuroinflammatory disorders, including Alzheimer's and Parkinson's diseases. Abnormal sphingolipid alterations, which involves an increase in ceramide and a decrease in sphingosine kinase, are observed during neuroinflammatory disease. These trends are observed early during disease development, and thus highlight the potential of sphingolipids as a new therapeutic and diagnostic target for neuroinflammatory diseases.

• Journal of Ginseng Research
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• 제48권1호
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• pp.20-30
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• 2024

Red ginseng (RG) is widely used as a herbal medicine. As the human lifespan has increased, numerous diseases have developed, and RG has also been used to treat various diseases. Neurodegenerative diseases are major problems that modern people face through their lives. Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis are featured by progressive nerve system damage. Recently, neuroinflammation has emerged as a degenerative factor and is an immune response in which cytokines with nerve cells that constitute the nervous system. RG, a natural herbal medicine with fewer side effects than chemically synthesized drugs, is currently in the spotlight. Therefore, we reviewed studies reporting the roles of RG in treating neuroinflammation and neurodegenerative diseases and found that RG might help alleviate neurodegenerative diseases by regulating neuroinflammation.

• BMB Reports
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• 제55권12호
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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.

• Nuclear Medicine and Molecular Imaging
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• 제42권sup1호
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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.

• 생명과학회지
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• 제33권9호
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• pp.736-745
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• 2023

노화란 세포 및 생리 기능이 점진적으로 손상되는 복잡한 과정이다. 알츠하이머, 동맥경화 및 갱년기와 같은 노화와 관련된 질병은 노화가 진행이 되면서 발생된다. 노화와 관련된 질환은 다양한 원인에 의해 발생된다. 그 중 유전적인 변화 없이 유전자 발현을 조절하는 후성유전의 변화는 노화, 그리고 노화와 관련된 질환의 발생에 중요한 조절자로 알려져있다. 이 리뷰에서는 후성유전의 변화가 노화 및 노화와 관련된 질병의 발전과 진행에 어떠한 역할을 하는지에 대해 서술하였다. 노화 중에 일어나는 유전적 변화의 분자적 기전과 이러한 변화가 노화와 관련된 질병에 미치는 영향, 특히 노화와 관련된 질환과 관련된 유전자 발현 양식을 조절하는 RNA 메틸화, DNA 메틸화 및 miRNA에 대해 중점적으로 초점을 맞추었다.

• 한국산학기술학회논문지
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• 제12권10호
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• pp.4411-4417
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• 2011

현대사회가 급속히 고령화됨에 따라 알츠하이머질환, 파킨슨병 등 퇴행성 뇌질환의 발생속도도 급증하고 있다. 퇴행성 뇌질환 대부분은 아직도 근원적인 치료가 불가능한 채 발병원인도 명확하지 않은 상태이나 최근 세포분자학적 기술 수준의 향상으로 퇴행성 뇌질환의 원인 규명 및 치료제 개발에 활기를 띠고 있다. 본 연구에서는 퇴행성 뇌질환 기작별 최근 치료제의 연구개발 동향과 국내외 기술동향을 조사 분석 하였으며, 과학계량학적 특허정보 분석을 통해 국가별 기술수준을 파악하고 기술개발 전망을 제시하였다.

• BMB Reports
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• 제49권6호
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• pp.337-343
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• 2016

Understanding of trafficking, processing, and degradation mechanisms of amyloid precursor protein (APP) is important because APP can be processed to produce β-amyloid (Aβ), a key pathogenic molecule in Alzheimer's disease (AD). Here, we found that APP contains KFERQ motif at its C-terminus, a consensus sequence for chaperone-mediated autophagy (CMA) or microautophagy which are another types of autophagy for degradation of pathogenic molecules in neurodegenerative diseases. Deletion of KFERQ in APP increased C-terminal fragments (CTFs) and secreted N-terminal fragments of APP and kept it away from lysosomes. KFERQ deletion did not abolish the interaction of APP or its cleaved products with heat shock cognate protein 70 (Hsc70), a protein necessary for CMA or microautophagy. These findings suggest that KFERQ motif is important for normal processing and degradation of APP to preclude the accumulation of APP-CTFs although it may not be important for CMA or microautophagy.

• Journal of Dairy Science and Biotechnology
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• 제38권3호
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• pp.134-141
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• 2020

Oxidative stress is a cascade reaction characterized by a significant increase in the amount of oxidized components. Free radicals produced by oxidative stress are one of the common features in several experimental models of disease, and contribute to wide range of neurodegenerative diseases, including Alzheimer's disease. Iron (II) species can participate in the Fenton, and Fenton-like reactions, to react with hydrogen peroxide and generate hydroxyl radical. As iron accumulation and oxidative stress are associated with the pathological progression of neurodegenerative diseases, iron chelation and antioxidant therapies have become strategies to combat these diseases. Due to the complexity of the redox system in vivo, a multifaceted approach may be an attractive therapeutic strategy. Further investigations are highly expected for the prevention and treatment of neurodegenerative diseases in future.

• BMB Reports
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• 제50권5호
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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).

• 한국멀티미디어학회논문지
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• 제20권2호
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• pp.205-215
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• 2017

The brain magnetic resonance images (MRI) is an important imaging biomarker in Alzheimer's disease (AD) as the cerebral atrophy has been shown to strongly associate with cognitive symptoms. The decrease of volume estimates in different structures of the medial temporal lobe related to memory correlates with the decline of cognitive functions in neurodegenerative diseases. During the past decades several methods have been developed for quantifying the disease related atrophy of hippocampus from MRI. Special effort has been dedicated to separate AD and mild cognitive impairment (MCI) related modifications from normal aging for the purpose of early detection and prediction. We trained a multi-class support vector machine (SVM) with probabilistic outputs on a sample (n = 58) of 20 normal controls (NC), 19 individuals with MCI, and 19 individuals with AD. The model was then applied to the cross-validation of same data set which no labels were known and the predictions. This study presents data on the association between MRI quantitative parameters of hippocampus and its quantitative structural changes examination use on the classification of the diseases.