본문 바로가기
KERD
논문KCI 등재

The role of cell type-specific mitochondrial dysfunction in the pathogenesis of Alzheimer’s disease

김동규|묵인희
생화학분자생물학회 (Korean Society Of Biochemistry And Molecular Biology)|2019.12|BMB Reports|제52권 제12호|pp. 679-688|DOI https://doi.org/10.5483/BMBRep.2019.52.12.282

1

조회

0

다운로드

1

인용

0

참고문헌

키워드

MitochondriaMitochondrial DysfunctionAlzheimer's DiseaseBioenergetic DefectsMitochondrial Dynamics
주제분류화학

초록

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.

Abstract

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.

참고문헌 (110)

  1. Querfurth HW, "Alzheimer's disease", N Engl J Med, 362, pp.329~344 (2010)
  2. Cao J, "Advances in developing novel therapeutic strategies for Alzheimer's disease", Mol Neurodegener, 13, pp.64~ (2018)
  3. Sanabria-Castro A, "Molecular Pathogenesis of Alzheimer's Disease : An Update", Ann Neurosci, 24, pp.46~54 (2017)
  4. Marcus C, "Brain PET in the diagnosis of Alzheimer's disease", Clin Nucl Med, 39, pp.e413~e422 (2014)[DOI]
  5. Mosconi L, "Pre-clinical detection of Alzheimer's disease using FDG-PET, with or without amyloid imaging", J Alzheimers Dis, 20, pp.843~854 (2010)
  6. Patel JR, "Age-related changes in neuronal glucose uptake in response to glutamate and beta-amyloid", J Neurosci Res, 72, pp.527~536 (2003)
  7. Beal MF, "Aging, energy, and oxidative stress in neurodegenerative diseases", Ann Neurol, 38, pp.357~366 (1995)
  8. Mancuso M, "Mitochondria, cognitive impairment, and Alzheimer's disease", Int J Alzheimers Dis, 2009, pp.951548~ (2009)
  9. Zhu X, "Abnormal mitochondrial dynamics in the pathogenesis of Alzheimer's disease", J Alzheimers Dis, 33(Suppl 1), pp.S253~S262 (2013)
  10. Wang X, "The role of abnormal mitochondrial dynamics in the pathogenesis of Alzheimer's disease", J Neurochem, 109(Suppl 1), pp.153~159 (2009)
  11. Swerdlow RH, "Mitochondria and Mitochondrial Cascades in Alzheimer's Disease", J Alzheimers Dis, 62, pp.1403~1416 (2018)
  12. Swerdlow RH, "The Alzheimer's disease mitochondrial cascade hypothesis", J Alzheimers Dis, 20(Suppl 2), pp.S265~S279 (2010)
  13. Swerdlow RH, "The Alzheimer's disease mitochondrial cascade hypothesis : progress and perspectives", Biochim Biophys Acta, 1842, pp.1219~1231 (2014)
  14. Cheng Y, "The Association of Tau With Mitochondrial Dysfunction in Alzheimer's Disease", Front Neurosci, 12, pp.163~ (2018)
  15. Reddy PH, "Amyloid beta, mitochondrial dysfunction and synaptic damage : implications for cognitive decline in aging and Alzheimer's disease", Trends Mol Med, 14, pp.45~53 (2008)
  16. Szablewski L, "Glucose Transporters in Brain : In Health and in Alzheimer's Disease", J Alzheimers Dis, 55, pp.1307~1320 (2017)
  17. Sun J, "Down-regulation of energy metabolism in Alzheimer's disease is a protective response of neurons to the microenvironment", J Alzheimers Dis, 28, pp.389~402 (2012)
  18. Sonntag KC, "Late-onset Alzheimer's disease is associated with inherent changes in bioenergetics profiles", Sci Rep, 7, pp.14038~ (2017)
  19. Carvalho C, "Metabolic alterations induced by sucrose intake and Alzheimer's disease promote similar brain mitochondrial abnormalities", Diabetes, 61, pp.1234~1242 (2012)
  20. Zhang C, "Characterization of ATP alternations in an Alzheimer's disease transgenic mouse model", J Alzheimers Dis, 44, pp.375~378 (2015)
  21. Cha MY, "Mitochondriaspecific accumulation of amyloid beta induces mitochondrial dysfunction leading to apoptotic cell death", PLoS One, 7, pp.e34929~ (2012)
  22. Keeney JT, "Human ApoE Isoforms Differentially Modulate Glucose and Amyloid Metabolic Pathways in Female Brain : Evidence of the Mechanism of Neuroprotection by ApoE2 and Implications for Alzheimer's Disease Prevention and Early Intervention", J Alzheimers Dis, 48, pp.411~424 (2015)
  23. Wu L, "Human ApoE Isoforms Differentially Modulate Brain Glucose and Ketone Body Metabolism : Implications for Alzheimer's Disease Risk Reduction and Early Intervention", J Neurosci, 38, pp.6665~6681 (2018)
  24. Rhein V, "Amyloid-beta leads to impaired cellular respiration, energy production and mitochondrial electron chain complex activities in human neuroblastoma cells", Cell Mol Neurobiol, 29, pp.1063~1071 (2009)
  25. Beck SJ, "Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer's disease", Nat Commun, 7, pp.11483~ (2016)
  26. David DC, "Proteomic and functional analyses reveal a mitochondrial dysfunction in P301L tau transgenic mice", J Biol Chem, 280, pp.23802~23814 (2005)
  27. Schulz KL, "A new link to mitochondrial impairment in tauopathies", Mol Neurobiol, 46, pp.205~216 (2012)
  28. Rhein V, "Amyloid-beta and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer's disease mice", Proc Natl Acad Sci U S A, 106, pp.20057~20062 (2009)
  29. Manczak M, "Mitochondria are a direct site of A beta accumulation in Alzheimer's disease neurons : implications for free radical generation and oxidative damage in disease progression", Hum Mol Genet, 15, pp.1437~1449 (2006)
  30. Caspersen C, "Mitochondrial Abeta : a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease", FASEB J, 19, pp.2040~2041 (2005)
  31. Devi L, "Accumulation of amyloid precursor protein in the mitochondrial import channels of human Alzheimer's disease brain is associated with mitochondrial dysfunction", J Neurosci, 26, pp.9057~9068 (2006)
  32. Hansson Petersen CA, "The amyloid beta-peptide is imported into mitochondria via the TOM import machinery and localized to mitochondrial cristae", Proc Natl Acad Sci U S A, 105, pp.13145~13150 (2008)
  33. Chen JX, "Role of mitochondrial amyloid-beta in Alzheimer's disease", J Alzheimers Dis, 20(Suppl 2), pp.S569~S578 (2010)
  34. Han SH, "Amyloid beta-interacting partners in Alzheimer's disease : From accomplices to possible therapeutic targets", Prog Neurobiol, 137, pp.17~38 (2016)
  35. Yoshida M, "ATP synthase--a marvellous rotary engine of the cell", Nat Rev Mol Cell Biol, 2, pp.669~677 (2001)
  36. Cha MY, "Mitochondrial ATP synthase activity is impaired by suppressed OGlcNAcylation in Alzheimer's disease", Hum Mol Genet, 24, pp.6492~6504 (2015)
  37. Halestrap A, "Biochemistry : a pore way to die", Nature, 434, pp.578~579 (2005)
  38. Nicotra A, "Apoptotic molecules and MPTP-induced cell death", Neurotoxicol Teratol, 24, pp.599~605 (2002)
  39. Zamzami N, "Mitochondrial permeability transition in apoptosis and necrosis", Cell Death Differ, 12(Suppl 2), pp.1478~1480 (2005)
  40. Javadov S, "Mitochondrial permeability transition and cell death : the role of cyclophilin d", Front Physiol, 4, pp.76~ (2013)
  41. Du H, "Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease", Nat Med, 14, pp.1097~1105 (2008)
  42. Lustbader JW, "ABAD directly links Abeta to mitochondrial toxicity in Alzheimer's disease", Science, 304, pp.448~452 (2004)
  43. Vogtle FN, "Global analysis of the mitochondrial N-proteome identifies a processing peptidase critical for protein stability", Cell, 139, pp.428~439 (2009)
  44. Mossmann D, "Amyloid-beta peptide induces mitochondrial dysfunction by inhibition of preprotein maturation", Cell Metab, 20, pp.662~669 (2014)
  45. Mishra P, "Metabolic regulation of mitochondrial dynamics", J Cell Biol, 212, pp.379~387 (2016)
  46. Youle RJ, "Mitochondrial fission, fusion, and stress", Science, 337, pp.1062~1065 (2012)
  47. Zhang L, "Altered brain energetics induces mitochondrial fission arrest in Alzheimer's Disease", Sci Rep, 6, pp.18725~ (2016)
  48. Shah SI, "Mitochondrial fragmentation and network architecture in degenerative diseases", PLoS One, 14, pp.e0223014~ (2019)
  49. Wang X, "Impaired balance of mitochondrial fission and fusion in Alzheimer's disease", J Neurosci, 29, pp.9090~9103 (2009)
  50. Tyumentsev MA, "Mitochondria with Morphology Characteristic for Alzheimer's Disease Patients Are Found in the Brain of OXYS Rats", Biochemistry (Mosc), 83, pp.1083~1088 (2018)
  51. Trushina E, "A shape shifting organelle : unusual mitochondrial phenotype determined with threedimensional electron microscopy reconstruction", Neural Regen Res, 11, pp.900~901 (2016)
  52. Xie H, "Mitochondrial alterations near amyloid plaques in an Alzheimer's disease mouse model", J Neurosci, 33, pp.17042~17051 (2013)
  53. Perez MJ, "Mitochondrial Bioenergetics Is Altered in Fibroblasts from Patients with Sporadic Alzheimer's Disease", Front Neurosci, 11, pp.553~ (2017)
  54. Manczak M, "Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease : implications for neuronal damage", Hum Mol Genet, 20, pp.2495~2509 (2011)
  55. Joshi AU, "Drp1", Fis1 interaction mediates mitochondrial dysfunction, bioenergetic failure and cognitive decline in Alzheimer's disease, 2018, pp.9, 6128~6143
  56. Baek SH, "Inhibition of Drp1Ameliorates Synaptic Depression, Abeta Deposition, and Cognitive Impairment in an Alzheimer's Disease Model", J Neurosci, 37, pp.5099~5110 (2017)
  57. Wang X, "Amyloid-beta overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission", fusion proteins, 2008, pp.105, 19318~19323
  58. Knott AB, "Mitochondrial fragmentation in neurodegeneration", Nat Rev Neurosci, 9, pp.505~518 (2008)
  59. Westermann B, "Nitric oxide links mitochondrial fission to Alzheimer's disease", Sci Signal, 2, pp.pe29~ (2009)
  60. Cho DH, "S-nitrosylation of Drp1 mediates beta-amyloid-related mitochondrial fission and neuronal injury", Science, 324, pp.102~105 (2009)
  61. Kang S, "Thrombospondin-1 protects against Abeta-induced mitochondrial fragmentation and dysfunction in hippocampal cells", Cell Death Discov, 4, pp.31~ (2018)
  62. Manczak M, "Abnormal interaction between the mitochondrial fission protein Drp1 and hyperphosphorylated tau in Alzheimer's disease neurons : implications for mitochondrial dysfunction and neuronal damage", Hum Mol Genet, 21, pp.2538~2547 (2012)
  63. Kandimalla R, "Reduced dynamin-related protein 1 protects against phosphorylated Tau-induced mitochondrial dysfunction and synaptic damage in Alzheimer's disease", Hum Mol Genet, 25, pp.4881~4897 (2016)
  64. Perez MJ, "Caspase-Cleaved Tau Impairs Mitochondrial Dynamics in Alzheimer's Disease", Mol Neurobiol, 55, pp.1004~1018 (2018)
  65. Byun J, "CR6-interacting factor 1 is a key regulator in Abeta-induced mitochondrial disruption and pathogenesis of Alzheimer's disease", Cell Death Differ, 22, pp.959~973 (2015)
  66. Kim C, "HDAC6 inhibitor blocks amyloid beta-induced impairment of mitochondrial transport in hippocampal neurons", PLoS One, 7, pp.e42983~ (2012)
  67. Shahpasand K, "Regulation of mitochondrial transport and inter-microtubule spacing by tau phosphorylation at the sites hyperphosphorylated in Alzheimer's disease", J Neurosci, 32, pp.2430~2441 (2012)
  68. Kopeikina KJ, "Tau accumulation causes mitochondrial distribution deficits in neurons in a mouse model of tauopathy and in human Alzheimer's disease brain", Am J Pathol, 179, pp.2071~2082 (2011)
  69. Stamer K, "Tau blocks traffic of organelles, neurofilaments, and APP vesicles in neurons and enhances oxidative stress", J Cell Biol, 156, pp.1051~1063 (2002)
  70. Fecher C, "Cell-typespecific profiling of brain mitochondria reveals functional and molecular diversity", Nat Neurosci, 22, pp.1731~1742 (2019)
  71. Ioannou MS, "Neuron-Astrocyte Metabolic Coupling Protects against Activity-Induced Fatty Acid Toxicity", Cell, 177, pp.1522~1535 (2019)[DOI]
  72. Park J, "Mitochondrial dynamics modulate the expression of pro-inflammatory mediators in microglial cells", J Neurochem, 127, pp.221~232 (2013)
  73. Orihuela R, "Microglial M1", M2 polarization and metabolic states, 2016, pp.173, 649~665
  74. Vos M, "Synaptic mitochondria in synaptic transmission and organization of vesicle pools in health and disease", Front Synaptic Neurosci, 2, pp.139~ (2010)
  75. Davey GP, "Energy thresholds in brain mitochondria. Potential involvement in neurodegeneration", J Biol Chem, 273, pp.12753~12757 (1998)
  76. Brown MR, "Synaptic mitochondria are more susceptible to Ca2+overload than nonsynaptic mitochondria", J Biol Chem, 281, pp.11658~11668 (2006)
  77. Zott B, "A vicious cycle of beta amyloid-dependent neuronal hyperactivation", Science, 365, pp.559~565 (2019)
  78. Du H, "Early deficits in synaptic mitochondria in an Alzheimer's disease mouse model", Proc Natl Acad Sci U S A, 107, pp.18670~18675 (2010)
  79. Pickett EK, "Regionspecific depletion of synaptic mitochondria in the brains of patients with Alzheimer's disease", Acta Neuropathol, 136, pp.747~757 (2018)
  80. Jadiya P, "Impaired mitochondrial calcium efflux contributes to disease progression in models of Alzheimer's disease", Nat Commun, 10, pp.3885~ (2019)
  81. Lee SH, "Impaired short-term plasticity in mossy fiber synapses caused by mitochondrial dysfunction of dentate granule cells is the earliest synaptic deficit in a mouse model of Alzheimer's disease", J Neurosci, 32, pp.5953~5963 (2012)
  82. Lee SH, "Presenilins regulate synaptic plasticity and mitochondrial calcium homeostasis in the hippocampal mossy fiber pathway", Mol Neurodegener, 12, pp.48~ (2017)
  83. Gazit N, "IGF-1 Receptor Differentially Regulates Spontaneous and Evoked Transmission via Mitochondria at Hippocampal Synapses", Neuron, 89, pp.583~597 (2016)
  84. Moloney AM, "Defects in IGF-1 receptor, insulin receptor and IRS-1", 2 in Alzheimer's disease indicate possible resistance to IGF-1 and insulin signalling, 2010, pp.31, 224~243
  85. Zhang B, "Alternations of central insulin-like growth factor-1 sensitivity in APP", PS1transgenic mice and neuronal models, 2013, pp.91, 717~725
  86. Allen NJ, "Cell Biology of Astrocyte-Synapse Interactions", Neuron, 96, pp.697~708 (2017)
  87. Rose CF, "Astrocyte glutamine synthetase : pivotal in health and disease", Biochem Soc Trans, 41, pp.1518~1524 (2013)
  88. Jackson JG, "Neuronal activity and glutamate uptake decrease mitochondrial mobility in astrocytes and position mitochondria near glutamate transporters", J Neurosci, 34, pp.1613~1624 (2014)
  89. Xu NJ, "Morphine withdrawal increases glutamate uptake and surface expression of glutamate transporter GLT1 at hippocampal synapses", J Neurosci, 23, pp.4775~4784 (2003)
  90. Genda EN, "Co-compartmentalization of the astroglial glutamate transporter, GLT-1, with glycolytic enzymes and mitochondria", J Neurosci, 31, pp.18275~18288 (2011)
  91. Canals S, "Metabolic challenge to glia activates an adenosine-mediated safety mechanism that promotes neuronal survival by delaying the onset of spreading depression waves", J Cereb Blood Flow Metab, 28, pp.1835~1844 (2008)
  92. Belanger M, "Brain energy metabolism : focus on astrocyte-neuron metabolic cooperation", Cell Metab, 14, pp.724~738 (2011)
  93. Bouzier-Sore AK, "Unraveling the complex metabolic nature of astrocytes", Front Cell Neurosci, 7, pp.179~ (2013)
  94. Fu W, "Bioenergetic mechanisms in astrocytes may contribute to amyloid plaque deposition and toxicity", J Biol Chem, 290, pp.12504~12513 (2015)
  95. Ebert D, "Energy contribution of octanoate to intact rat brain metabolism measured by 13C nuclear magnetic resonance spectroscopy", J Neurosci, 23, pp.5928~5935 (2003)
  96. Jones VC, "Aberrant iPSC-derived human astrocytes in Alzheimer's disease", Cell Death Dis, 8, pp.e2696~ (2017)
  97. Oksanen M, "PSEN1 Mutant iPSC-Derived Model Reveals Severe Astrocyte Pathology in Alzheimer's Disease", Stem Cell Reports, 9, pp.1885~1897 (2017)
  98. Sekar S, "Alzheimer's disease is associated with altered expression of genes involved in immune response and mitochondrial processes in astrocytes", Neurobiol Aging, 36, pp.583~591 (2015)
  99. Myung NH, "Evidence of DNA damage in Alzheimer disease: phosphorylation of histone H2AX in astrocytes", Age (Dordr), 30, pp.209~215 (2008)
  100. Simpson JE, "Population variation in oxidative stress and astrocyte DNA damage in relation to Alzheimer-type pathology in the ageing brain", Neuropathol Appl Neurobiol, 36, pp.25~40 (2010)
  101. Lee HP, "Early induction of oxidative stress in mouse model of Alzheimer disease with reduced mitochondrial superoxide dismutase activity", PLoS One, 7, pp.e28033~ (2012)
  102. Sarkar P, "Epoxyeicosatrienoic acids pretreatment improves amyloid beta-induced mitochondrial dysfunction in cultured rat hippocampal astrocytes", Am J Physiol Heart Circ Physiol, 306, pp.H475~H484 (2014)
  103. Abeti R, "Beta-amyloid activates PARP causing astrocytic metabolic failure and neuronal death", Brain, 134, pp.1658~1672 (2011)
  104. Abramov AY, "Beta-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase", J Neurosci, 24, pp.565~575 (2004)
  105. Culmsee C, "Mitochondria, Microglia, and the Immune System-How Are They Linked in Affective Disorders?", Front Psychiatry, 9, pp.739~ (2018)
  106. Baik SH, "A Breakdown in Metabolic Reprogramming Causes Microglia Dysfunction in Alzheimer's Disease", Cell Metab, 30, pp.493~507 (2019)[DOI]
  107. Konttinen H, "PSEN1DeltaE9, APPswe, and APOE4 Confer Disparate Phenotypes in Human iPSC-Derived Microglia", Stem Cell Reports, 13, pp.669~683 (2019)
  108. Ulland TK, "TREM2Maintains Microglial Metabolic Fitness in Alzheimer's Disease", Cell, 170, pp.649~663 (2017)[DOI]
  109. Joshi AU, "Fragmented mitochondria released from microglia trigger A1 astrocytic response and propagate inflammatory neurodegeneration", Nat Neurosci, 22, pp.1635~1648 (2019)
  110. Fang EF, "Mitophagy inhibits amyloid-beta and tau pathology and reverses cognitive deficits in models of Alzheimer's disease", Nat Neurosci, 22, pp.401~412 (2019)

관련 논문AI추천

Emerging perspectives on mitochondrial dysfunction and inflammation in Alzheimer’s disease김서현, 박지수, Seung-Min Yoo, Yong-Keun Jung생화학분자생물학회 · BMB Reports2020 · 제53권 제1호Dysfunctional Mitochondrial Bioenergetics and Synaptic Degeneration in Alzheimer DiseaseAlfredo Oliveros, Jason Tang, Mi Hyeon Jang대한배뇨장애요실금학회 · International Neurourology Journal2019 · 제23권 제1호Mitochondrial dysfunction and Alzheimer’s disease: prospects for therapeutic intervention이지연, Ae Nim Pae, Ji Woong Lim생화학분자생물학회 · BMB Reports2020 · 제53권 제1호Mitochondrial Complex I Inhibition Accelerates Amyloid Toxicity조예찬, 최원석한국발생생물학회 · 발생과 생식2017 · 제21권 제4호Pathological phenotypes of astrocytes in Alzheimer’s disease유익동, 임재준, Kim Junhyung, Moon Jong-Seok생화학분자생물학회 · Experimental and Molecular Medicine2024 · 제56권 Cellular and Molecular Mediators of Neuroinflammation in Alzheimer Disease양승훈대한배뇨장애요실금학회 · International Neurourology Journal2019 · 제23권 제1호

이 간행물의 다른 논문 (6건)

The Yin and Yang of RNA surveillance in B lymphocytes and antibody-secreting plasma cellsJean-Marie Lambert, Nivine Srour, Laurent Delpypp. 671-678Mitochondrial genome mutations in mesenchymal stem cells derived from human dental induced pluripotent stem cells김덕훈, 신주성, 노규진, 박봉욱, 박주미, 이현정, 강은주, 이연미, 손영범pp. 689-694Transduced Tat-CIAPIN1 reduces the inflammatory response on LPS- and TPA-induced damages여현지, 김민영, 김정수, 신민재, 김덕수, 최수영, 김대원, 유지호, 엄원식pp. 695-699LIR motifs and the membrane-targeting domain are complementary in the function of RavZ전용우, 전푸름, 박상원, 이유경, 이승환, 박주희, 이진아, 장덕진pp. 700-705Inhibition of p90RSK activation sensitizes triple-negative breast cancer cells to cisplatin by inhibiting proliferation, migration and EMT허경선, 명창선, Diem Thi Ngoc Huynh, 진유진, 강건욱pp. 706-711
원문 보기