• 제목/요약/키워드: Neurodegenerative disease

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Biomedical Application of Phosphoproteomics in Neurodegenerative Diseases

  • Bahk, Young Yil;Mohamed, Bari;Kim, Young Jun
    • Journal of Microbiology and Biotechnology
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    • 제23권3호
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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.

퇴행성 뇌질환에서 뇌 자기공명영상 기반 인공지능 소프트웨어 활용의 현재 (Brain MRI-Based Artificial Intelligence Software in Patients with Neurodegenerative Diseases: Current Status)

  • 정소영;서종현;박호영;허훤;심우현;김상준
    • 대한영상의학회지
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    • 제83권3호
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    • pp.473-485
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    • 2022
  • 현대사회가 점차 고령화 사회가 됨에 따라 퇴행성 뇌질환의 발병률이 증가하고 있으며, 이러한 퇴행성 뇌질환에 관한 많은 연구들이 이루어지고 있다. 퇴행성 뇌질환의 진단에서 영상분석은 영상표지자로서 중요한 역할을 하고 있다. 영상분석에서 객관적이고 일관성 있는 평가는 퇴행성 뇌질환의 조기 진단 및 정확한 진단에 중요하다. 이에 다양한 퇴행성 뇌질환과 관련한 영상연구에 자기공명영상(이하 MRI)을 이용한 인공지능이 조기 진단과 최적의 치료 방향 계획 및 결정에 도움이 될 가능성을 보여주었다. 특히 MRI 기반의 뇌용적 측정과 분획화 및 특성을 포착하는 인공지능 소프트웨어들이 개발되고 연구되기 시작했다. 본 고찰에서는 우리나라에서 퇴행성 뇌질환과 관련하여 사용되고 있는 인공지능 소프트웨어의 현재 상황과 향후 인공지능 소프트웨어의 퇴행성 뇌질환 연구에의 활용, 그리고 인공지능 소프트웨어의 한계에 대해서 다루고자 한다.

Autophagy in neurodegeneration: two sides of the same coin

  • Lee, Jin-A
    • BMB Reports
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    • 제42권6호
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    • pp.324-330
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    • 2009
  • Autophagy is a bulk lysosomal degradation process important in development, differentiation and cellular homeostasis in multiple organs. Interestingly, neuronal survival is highly dependent on autophagy due to its post-mitotic nature, polarized morphology and active protein trafficking. A growing body of evidence now suggests that alteration or dysfunction of autophagy causes accumulation of abnormal proteins and/or damaged organelles, thereby leading to neurodegenerative disease. Although autophagy generally prevents neuronal cell death, it plays a protective or detrimental role in neurodegenerative disease depending on the environment. In this review, the two sides of autophagy will be discussed in the context of several neurodegenerative diseases.

Patient-specific pluripotent stem cell-based Parkinson's disease models showing endogenous alpha-synuclein aggregation

  • Oh, Yohan
    • BMB Reports
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    • 제52권6호
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    • pp.349-359
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    • 2019
  • After the first research declaring the generation of human induced pluripotent stem cells (hiPSCs) in 2007, several attempts have been made to model neurodegenerative disease in vitro during the past decade. Parkinson's disease (PD) is the second most common neurodegenerative disorder, which is mainly characterized by motor dysfunction. The formation of unique and filamentous inclusion bodies called Lewy bodies (LBs) is the hallmark of both PD and dementia with LBs. The key pathology in PD is generally considered to be the alpha-synuclein (${\alpha}$-syn) accumulation, although it is still controversial whether this protein aggregation is a cause or consequence of neurodegeneration. In the present work, the recently published researches which recapitulated the ${\alpha}$-syn aggregation phenomena in sporadic and familial PD hiPSC models were reviewed. Furthermore, the advantages and potentials of using patient-derived PD hiPSC with focus on ${\alpha}$-syn aggregation have been discussed.

근위축측삭경화증에 대한 치료약물 임상시험 현황 (Update of Therapeutic Clinical Trials for Amyotrophic Lateral Sclerosis)

  • 김남희;이민오
    • Annals of Clinical Neurophysiology
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    • 제17권1호
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    • pp.1-16
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    • 2015
  • Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is characterized by progressive death of motor neurons in the cortex, brainstem, and spinal cord. Until now, many treatment strategies have been tested in ALS, but so far only Riluzole has shown efficacy of slightly slowing disease progression. The pathophysiological mechanisms underlying ALS are multifactorial, with a complex interaction between genetic factors and molecular pathways. Other motor neuron disease such as spinal muscular atrophy (SMA) and spinobulbar muscular atrophy (SBMA) are also progressive neurodegenerative disease with loss of motor neuron as ALS. This common thread of motor neuron loss has provided a target for the development of therapies for these motor neuron diseases. A better understanding of these pathogenic mechanisms and the potential pathological relationship between the various cellular processes have suggested novel therapeutic approaches, including stem cell and genetics-based strategies, providing hope for feasible treatment of ALS.

Neuroprotective roles of pituitary adenylate cyclase-activating polypeptide in neurodegenerative diseases

  • Lee, Eun Hye;Seo, Su Ryeon
    • BMB Reports
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    • 제47권7호
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    • pp.369-375
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    • 2014
  • Pituitary adenylate cyclase-activating polypeptide (PACAP) is a pleiotropic bioactive peptide that was first isolated from an ovine hypothalamus in 1989. PACAP belongs to the secretin/glucagon/vasoactive intestinal polypeptide (VIP) superfamily. PACAP is widely distributed in the central and peripheral nervous systems and acts as a neurotransmitter, neuromodulator, and neurotrophic factor via three major receptors (PAC1, VPAC1, and VPAC2). Recent studies have shown a neuroprotective role of PACAP using in vitro and in vivo models. In this review, we briefly summarize the current findings on the neurotrophic and neuroprotective effects of PACAP in different brain injury models, such as cerebral ischemia, Parkinson's disease (PD), and Alzheimer's disease (AD). This review will provide information for the future development of therapeutic strategies in treatment of these neurodegenerative diseases.

MicroRNAs in Human Diseases: From Autoimmune Diseases to Skin, Psychiatric and Neurodegenerative Diseases

  • Ha, Tai-You
    • IMMUNE NETWORK
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    • 제11권5호
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    • pp.227-244
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    • 2011
  • MicroRNAs (miRNAs) are small noncoding RNA molecules that negatively regulate gene expression via degradation or translational repression of their target messenger RNAs (mRNAs). Recent studies have clearly demonstrated that miRNAs play critical roles in several biologic processes, including cell cycle, differentiation, cell development, cell growth, and apoptosis and that miRNAs are highly expressed in regulatory T (Treg) cells and a wide range of miRNAs are involved in the regulation of immunity and in the prevention of autoimmunity. It has been increasingly reported that miRNAs are associated with various human diseases like autoimmune disease, skin disease, neurological disease and psychiatric disease. Recently, the identification of miRNAs in skin has added a new dimension in the regulatory network and attracted significant interest in this novel layer of gene regulation. Although miRNA research in the field of dermatology is still relatively new, miRNAs have been the subject of much dermatological interest in skin morphogenesis and in regulating angiogenesis. In addition, miRNAs are moving rapidly center stage as key regulators of neuronal development and function in addition to important contributions to neurodegenerative disorder. Moreover, there is now compelling evidence that dysregulation of miRNA networks is implicated in the development and onset of human neruodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, Tourette's syndrome, Down syndrome, depression and schizophrenia. In this review, I briefly summarize the current studies about the roles of miRNAs in various autoimmune diseases, skin diseases, psychoneurological disorders and mental stress.

산화스트레스와 치매 (Oxidative Stress and Alzheimer's Disease)

  • 유자연;윤정희;설국환;오미화;함준상
    • 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.

New insight into transglutaminase 2 and link to neurodegenerative diseases

  • Min, Boram;Chung, Kwang Chul
    • BMB Reports
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    • 제51권1호
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    • pp.5-13
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    • 2018
  • Formation of toxic protein aggregates is a common feature and mainly contributes to the pathogenesis of neurodegenerative diseases (NDDs), which include amyotrophic lateral sclerosis (ALS), Alzheimer's, Parkinson's, Huntington's, and prion diseases. The transglutaminase 2 (TG2) gene encodes a multifunctional enzyme, displaying four types of activity, such as transamidation, GTPase, protein disulfide isomerase, and protein kinase activities. Many studies demonstrated that the calcium-dependent transamidation activity of TG2 affects the formation of insoluble and toxic amyloid aggregates that mainly consisted of NDD-related proteins. So far, many important and NDD-related substrates of TG2 have been identified, including $amlyoid-{\beta}$, tau, ${\alpha}-synuclein$, mutant huntingtin, and ALS-linked trans-activation response (TAR) DNA-binding protein 43. Recently, the formation of toxic inclusions mediated by several TG2 substrates were efficiently inhibited by TG2 inhibitors. Therefore, the development of highly specific TG2 inhibitors would be an important tool in alleviating the progression of TG2-related brain disorders. In this review, the authors discuss recent advances in TG2 biochemistry, several mechanisms of molecular regulation and pleotropic signaling functions, and the presumed role of TG2 in the progression of many NDDs.

Emerging signals modulating potential of ginseng and its active compounds focusing on neurodegenerative diseases

  • Jakaria, Md.;Kim, Joonsoo;Karthivashan, Govindarajan;Park, Shin-Young;Ganesan, Palanivel;Choi, Dong-Kug
    • Journal of Ginseng Research
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    • 제43권2호
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    • pp.163-171
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    • 2019
  • Common features of neurodegenerative diseases (NDDs) include progressive dysfunctions and neuronal injuries leading to deterioration in normal brain functions. At present, ginseng is one of the most frequently used natural products. Its use has a long history as a cure for various diseases because its extracts and active compounds exhibit several pharmacological properties against several disorders. However, the pathophysiology of NDDs is not fully clear, but researchers have found that various ion channels and specific signaling pathways might have contributed to the disease pathogenesis. Apart from the different pharmacological potentials, ginseng and its active compounds modulate various ion channels and specific molecular signaling pathways related to the nervous system. Here, we discuss the signal modulating potential of ginseng and its active compounds mainly focusing on those relevant to NDDs.