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      KCI등재 SCOPUS SCIE

      Quantitative Proteomic Analysis Reveals Impaired Axonal Guidance Signaling in Human Postmortem Brain Tissues of Chronic Traumatic Encephalopathy

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      https://www.riss.kr/link?id=A106279676

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      다국어 초록 (Multilingual Abstract)

      Chronic traumatic encephalopathy (CTE) is a distinct neurodegenerative disease that associated with repetitive head trauma. CTE is neuropathologically defined by the perivascular accumulation of abnormally phosphorylated tau protein in the depths of the sulci in the cerebral cortices. In advanced CTE, hyperphosphorylated tau protein deposits are found in widespread regions of brain, however the mechanisms of the progressive neurodegeneration in CTE are not fully understood. In order to identify which proteomic signatures are associated with CTE, we prepared RIPA-soluble fractions and performed quantitative proteomic analysis of postmortem brain tissue from individuals neuropathologically diagnosed with CTE. We found that axonal guidance signaling pathwayrelated proteins were most significantly decreased in CTE. Immunohistochemistry and Western blot analysis showed that axonal signaling pathway-related proteins were down regulated in neurons and oligodendrocytes and neuron-specific cytoskeletal proteins such as TUBB3 and CFL1 were reduced in the neuropils and cell body in CTE. Moreover, oligodendrocyte-specific proteins such as MAG and TUBB4 were decreased in the neuropils in both gray matter and white matter in CTE, which correlated with the degree of axonal injury and degeneration. Our findings indicate that deregulation of axonal guidance proteins in neurons and oligodendrocytes is associated with the neuropathology in CTE. Together, altered axonal guidance proteins may be potential pathological markers for CTE.
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      Chronic traumatic encephalopathy (CTE) is a distinct neurodegenerative disease that associated with repetitive head trauma. CTE is neuropathologically defined by the perivascular accumulation of abnormally phosphorylated tau protein in the depths of t...

      Chronic traumatic encephalopathy (CTE) is a distinct neurodegenerative disease that associated with repetitive head trauma. CTE is neuropathologically defined by the perivascular accumulation of abnormally phosphorylated tau protein in the depths of the sulci in the cerebral cortices. In advanced CTE, hyperphosphorylated tau protein deposits are found in widespread regions of brain, however the mechanisms of the progressive neurodegeneration in CTE are not fully understood. In order to identify which proteomic signatures are associated with CTE, we prepared RIPA-soluble fractions and performed quantitative proteomic analysis of postmortem brain tissue from individuals neuropathologically diagnosed with CTE. We found that axonal guidance signaling pathwayrelated proteins were most significantly decreased in CTE. Immunohistochemistry and Western blot analysis showed that axonal signaling pathway-related proteins were down regulated in neurons and oligodendrocytes and neuron-specific cytoskeletal proteins such as TUBB3 and CFL1 were reduced in the neuropils and cell body in CTE. Moreover, oligodendrocyte-specific proteins such as MAG and TUBB4 were decreased in the neuropils in both gray matter and white matter in CTE, which correlated with the degree of axonal injury and degeneration. Our findings indicate that deregulation of axonal guidance proteins in neurons and oligodendrocytes is associated with the neuropathology in CTE. Together, altered axonal guidance proteins may be potential pathological markers for CTE.

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      참고문헌 (Reference)

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      2 Johnson VE, "Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?" 11 : 361-370, 2010

      3 서정선, "Transcriptome analyses of chronic traumatic encephalopathy show alterations in protein phosphatase expression associated with tauopathy" 생화학분자생물학회 49 : 1-12, 2017

      4 McKee AC, "The spectrum of disease in chronic traumatic encephalopathy" 136 : 43-64, 2013

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      1 Christman CW, "Ultrastructural studies of diffuse axonal injury in humans" 11 : 173-186, 1994

      2 Johnson VE, "Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?" 11 : 361-370, 2010

      3 서정선, "Transcriptome analyses of chronic traumatic encephalopathy show alterations in protein phosphatase expression associated with tauopathy" 생화학분자생물학회 49 : 1-12, 2017

      4 McKee AC, "The spectrum of disease in chronic traumatic encephalopathy" 136 : 43-64, 2013

      5 Finkelstein E, "The incidence and economic burden of injuries in the United States" Oxford University Press 2006

      6 McKee AC, "The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy" 131 : 75-86, 2016

      7 Thunnan DJ, "The epidemiology of sports-related traumatic brain injuries in the United States : recent developments" 13 : 1-8, 1998

      8 Langlois JA, "The epidemiology and impact of traumatic brain injury : a brief overview" 21 : 375-378, 2006

      9 Graves AB, "The association between head trauma and Alzheimer's disease" 131 : 491-501, 1990

      10 Szklarczyk D, "The STRING database in 2011: functional interaction networks of proteins, globally integrated and scored" 39 : D561-D568, 2011

      11 McKee AC, "TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathy" 69 : 918-929, 2010

      12 Su N, "Quantitative proteomic analysis of differentially expressed proteins and downstream signaling pathways in chronic bladder ischemia" 195 : 515-523, 2016

      13 Maxwell WL, "Post-acute alterations in the axonal cytoskeleton after traumatic axonal injury" 20 : 151-168, 2003

      14 Takase H, "Oligodendrogenesis after traumatic brain injury" 340 : 205-211, 2018

      15 Bradl M, "Oligodendrocytes : biology and pathology" 119 : 37-53, 2010

      16 Dent KA, "Oligodendrocyte birth and death following traumatic brain injury in adult mice" 10 : e0121541-, 2015

      17 Pomicter AD, "Nfasc155H and MAG are specifically susceptible to detergent extraction in the absence of the myelin sphingolipid sulfatide" 38 : 2490-2502, 2013

      18 Flygt J, "Myelin loss and oligodendrocyte pathology in white matter tracts following traumatic brain injury in the rat" 38 : 2153-2165, 2013

      19 Armstrong RC, "Myelin and oligodendrocyte lineage cells in white matter pathology and plasticity after traumatic brain injury" 110 : 654-659, 2016

      20 Poirier K, "Mutations in the neuronal β-tubulin subunit TUBB3 result in malformation of cortical development and neuronal migration defects" 19 : 4462-4473, 2010

      21 Marklund N, "Monitoring of brain interstitial total tau and beta amyloid proteins by microdialysis in patients with traumatic brain injury" 110 : 1227-1237, 2009

      22 Lee J, "Mitochondrial cyclic AMP response element-binding protein(CREB)mediates mitochondrial gene expression and neuronal survival" 280 : 40398-40401, 2005

      23 Greer JE, "Mild traumatic brain injury in the mouse induces axotomy primarily within the axon initial segment" 126 : 59-74, 2013

      24 Chung RS, "Mild axonal stretch injury in vitro induces a progressive series of neurofilament alterations ultimately leading to delayed axotomy" 22 : 1081-1091, 2005

      25 Baas PW, "Microtubule stability in the axon : new answers to an old mystery" 78 : 3-5, 2013

      26 Conde C, "Microtubule assembly, organization and dynamics in axons and dendrites" 10 : 319-332, 2009

      27 Cherry JD, "Microglial neuroinflammation contributes to tau accumulation in chronic traumatic encephalopathy" 4 : 112-, 2016

      28 Marner L, "Marked loss of myelinated nerve fibers in the human brain with age" 462 : 144-152, 2003

      29 Maxwell WL, "Loss of axonal microtubules and neurofilaments after stretch-injury to guinea pig optic nerve fibers" 14 : 603-614, 1997

      30 Chen XH, "Long-term accumulation of amyloid-beta, beta-secretase, presenilin-1, and caspase-3 in damaged axons following brain trauma" 165 : 357-371, 2004

      31 Staal JA, "Initial calcium release from intracellular stores followed by calcium dysregulation is linked to secondary axotomy following transient axonal stretch injury" 112 : 1147-1155, 2010

      32 Tischfield MA, "Human TUBB3 mutations perturb microtubule dynamics, kinesin interactions, and axon guidance" 140 : 74-87, 2010

      33 Deng W, "HemI: a toolkit for illustrating heatmaps" 9 : e111988-, 2014

      34 Mortimer JA, "Head trauma as a risk factor for Alzheimer's disease: a collaborative re-analysis of case-control studies" 20 (20): S28-S35, 1991

      35 Fleminger S, "Head injury as a risk factor for Alzheimer's disease : the evidence 10 years on; a partial replication" 74 : 857-862, 2003

      36 Mortimer JA, "Head injury as a risk factor for Alzheimer's disease" 35 : 264-267, 1985

      37 Guo Z, "Head injury and the risk of AD in the MIRAGE study" 54 : 1316-1323, 2000

      38 O'Meara ES, "Head injury and risk of Alzheimer's disease by apolipoprotein E genotype" 146 : 373-384, 1997

      39 Demer JL, "Evidence of an asymmetrical endophenotype in congenital fibrosis of extraocular muscles type 3 resulting from TUBB3mutations" 51 : 4600-4611, 2010

      40 Plassman BL, "Documented head injury in early adulthood and risk of Alzheimer's disease and other dementias" 55 : 1158-1166, 2000

      41 Shi H, "Demyelination as a rational therapeutic target for ischemic or traumatic brain injury" 272 : 17-25, 2015

      42 Tran HT, "Controlled cortical impact traumatic brain injury in 3xTg-AD mice causes acute intra-axonal amyloid-β accumulation and independently accelerates the development of tau abnormalities" 31 : 9513-9525, 2011

      43 Tagge CA, "Concussion, microvascular injury, and early tauopathy in young athletes after impact head injury and an impact concussion mouse model" 141 : 422-458, 2018

      44 Mez J, "Clinicopathological evaluation of chronic traumatic encephalopathy in players of American football" 318 : 360-370, 2017

      45 Stern RA, "Clinical presentation of chronic traumatic encephalopathy" 81 : 1122-1129, 2013

      46 Goldstein LE, "Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model" 4 : 134-, 2012

      47 McKee AC, "Chronic traumatic encephalopathy in athletes : progressive tauopathy after repetitive head injury" 68 : 709-735, 2009

      48 Omalu BI, "Chronic traumatic encephalopathy in a national football league player : part II" 59 : 1086-1092, 2006

      49 Omalu BI, "Chronic traumatic encephalopathy in a National Football League player" 57 : 128-134, 2005

      50 Omalu B, "Chronic traumatic encephalopathy" 28 : 38-49, 2014

      51 Pettus EH, "Characterization of a distinct set of intra-axonal ultrastructural changes associated with traumatically induced alteration in axolemmal permeability" 722 : 1-11, 1996

      52 Stone JR, "Caspase-3-mediated cleavage of amyloid precursor protein and formation of amyloid beta peptide in traumatic axonal injury" 19 : 601-614, 2002

      53 Cherry JD, "CCL11 is increased in the CNS in chronic traumatic encephalopathy but not in Alzheimer's disease" 12 : e0185541-, 2017

      54 Johnson VE, "Axonal pathology in traumatic brain injury" 246 : 35-43, 2013

      55 Jafari SS, "Axonal cytoskeletal changes after non-disruptive axonal injury" 26 : 207-221, 1997

      56 Coleman M, "Axon degeneration mechanisms : commonality amid diversity" 6 : 889-898, 2005

      57 Bradke F, "Assembly of a new growth cone after axotomy : the precursor to axon regeneration" 13 : 183-193, 2012

      58 Ryu H, "Antioxidants modulate mitochondrial PKA and increase CREB binding to D-loop DNA of the mitochondrial genome in neurons" 102 : 13915-13920, 2005

      59 Smith DH, "Amyloid beta accumulation in axons after traumatic brain injury in humans" 98 : 1072-1077, 2003

      60 Smith DH, "Accumulation of amyloid beta and tau and the formation of neurofilament inclusions following diffuse brain injury in the pig" 58 : 982-992, 1999

      61 Chen XH, "A lack of amyloid beta plaques despite persistent accumulation of amyloid beta in axons of long-term survivors of traumatic brain injury" 19 : 214-223, 2009

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2015-01-01 평가 등재학술지 선정 (계속평가) KCI등재
      2013-01-01 평가 등재후보 1차 FAIL (등재후보1차) KCI등재후보
      2012-01-01 평가 등재후보학술지 유지 (기타) KCI등재후보
      2010-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.25 0.25 0.22
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.2 0.19 0.459 0.05
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