알츠하이머 병과 글루타메이트성 시냅스 단백질의 분자적 질환 기전

키워드

참고문헌 (90)

1. Querfurth HW, "Alzheimer’s disease", N Engl J Med, 362, pp.329~344 (2010)
2. Levy-Lahad E, "Candidate gene for the chromosome 1 familial Alzheimer’s disease locus", Science, 269, pp.973~977 (1995)
3. Goate A, "Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer’s disease", Nature, 349, pp.704~706 (1991)
4. Nussbaum RL, "Alzheimer’s disease and Parkinson’s disease", N Engl J Med, 348, pp.1356~1364 (2003)
5. Corder EH, "Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families", Science, 261, pp.921~923 (1993)
6. Brose N, "Synaptopathy: dysfunction of synaptic function?", Biochem Soc Trans, 38, pp.443~444 (2010)
7. Selkoe DJ, "Alzheimer’s disease is a synaptic failure", Science, 298, pp.789~791 (2002)
8. Hsieh H, "AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss", Neuron, 52, pp.831~843 (2006)
9. Lacor PN, "Abeta oligomer-induced aberrations in synapse composition, shape, and density provide a molecular basis for loss of connectivity in Alzheimer’s disease", J Neurosci, 27, pp.796~807 (2007)
10. Opazo P, "A three-step model for the synaptic recruitment of AMPA receptors", Mol Cell Neurosci (2010)
11. Lin YC, "Mechanisms of synapse and dendrite maintenance and their disruption in psychiatric and neurodegenerative disorders", Annu Rev Neurosci, 33, pp.349~378 (2010)
12. Sheng M, "Postsynaptic signaling and plasticity mechanisms", Science, 298, pp.776~780 (2002)
13. Nimchinsky EA, "Structure and function of dendritic spines", Annu Rev Physiol, 64, pp.313~353 (2002)
14. Tada T, "Molecular mechanisms of dendritic spine morphogenesis", Curr Opin Neurobiol, 16, pp.95~101 (2006)
15. Sheng M, "The postsynaptic architecture of excitatory synapses: a more quantitative view", Annu Rev Biochem, 76, pp.823~847 (2007)
16. Baude A, "The metabotropic glutamate receptor( mGluR1 alpha) is concentrated at perisynaptic membrane of neuronal subpopulations as detected by immunogold reaction", Neuron, 11, pp.771~787 (1993)
17. Takumi Y, "Different modes of expression of AMPA and NMDA receptors in hippocampal synapses", Nat Neurosci, 2, pp.618~624 (1999)
18. Matsuzaki M, "Structural basis of long-term potentiation in single dendritic spines", Nature, 429, pp.761~766 (2004)
19. Bliss TV, "Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path", J Physiol, 232, pp.331~356 (1973)
20. Malenka RC, "LTP and LTD: an embarrassment of riches", Neuron, 44, pp.5~21 (2004)
21. Whitlock JR, "Learning induces long-term potentiation in the hippocampus", Science, 313, pp.1093~1097 (2006)
22. Massey PV, "Long-term depression: multiple forms and implications for brain function", Trends Neurosci, 30, pp.176~184 (2007)
23. Selkoe DJ, "Alzheimer’s disease: molecular understanding predicts amyloid-based therapeutics", Annu Rev Pharmacol Toxicol, 43, pp.545~584 (2003)
24. Na¨slund J, "Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline", JAMA, 283, pp.1571~1577 (2000)
25. DeKosky ST, "Synapse loss in frontal cortex biopsies in Alzheimer's disease: correlation with cognitive severity", Ann Neurol, 27, pp.457~464 (1990)
26. McLean CA, "Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer’s disease", Ann Neurol, 46, pp.860~866 (1999)
27. Terry RD, "Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment", Ann Neurol, 30, pp.572~580 (1991)
28. Mucke L, "High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation", J Neurosci, 20, pp.4050~4058 (2000)
29. Haass C, "Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer’s amyloid beta-peptide", Nat Rev Mol Cell Biol, 8, pp.101~112 (2007)
30. Selkoe DJ, "Alzheimer’s disease: genes, proteins, and therapy", Physiol Rev, 81, pp.741~766 (2001)
31. Tanzi RE, "Twenty years of the Alzheimer’s disease amyloid hypothesis: a genetic perspective", Cell, 120, pp.545~555 (2005)
32. Walsh DM, "A beta oligomers - a decade of discovery", J Neurochem, 101, pp.1172~1184 (2007)
33. Kanemitsu H, "Human neprilysin is capable of degrading amyloid beta peptide not only in the monomeric form but also the pathological oligomeric form", Neurosci Lett, 350, pp.113~116 (2003)
34. Iwata N, "Metabolic regulation of brain Abeta by neprilysin", Science, 292, pp.1550~1552 (2001)
35. Qiu WQ, "Insulin-degrading enzyme regulates extracellular levels of amyloid beta-protein by degradation", J Biol Chem, 273, pp.32730~32738 (1998)
36. Farris W, "Insulin-degrading enzyme regulates the levels of insulin, amyloid beta-protein, and the beta-amyloid precursor protein intracellular domain in vivo", Proc Natl Acad Sci U S A, 100, pp.4162~4167 (2003)
37. Kamenetz F, "APP processing and synaptic function", Neuron, 37, pp.925~937 (2003)
38. Scheff SW, "Synaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment", Neurology, 68, pp.1501~1508 (2007)
39. Masliah E, "Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease", Neurology, 56, pp.127~129 (2001)
40. Cullen WK, "Block of LTP in rat hippocampus in vivo by beta-amyloid precursor protein fragments", Neuroreport, 8, pp.3213~3217 (1997)
41. Walsh DM, "Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal longterm potentiation in vivo", Nature, 416, pp.535~539 (2002)
42. Roselli F, "Soluble beta-amyloid1-40 induces NMDA-dependent degradation of postsynaptic density-95 at glutamatergic synapses", J Neurosci, 25, pp.11061~11070 (2005)
43. Zhao D, "Amyloid beta prevents activation of calcium", calmodulin-dependent protein kinase II and AMPA receptor phosphorylation during hippocampal long-term potentiation, 2004, pp.92, 2853~2858
44. Townsend M, "Soluble Abeta inhibits specific signal transduction cascades common to the insulin receptor pathway", J Biol Chem, 282, pp.33305~33312 (2007)
45. Wei W, "Amyloid beta from axons and dendrites reduces local spine number and plasticity", Nat Neurosci, 13, pp.190~196 (2010)
46. Li S, "Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake", Neuron, 62, pp.788~801 (2009)
47. Shankar GM, "Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway", J Neurosci, 27, pp.2866~2875 (2007)
48. Shankar GM, "Amyloid-beta protein dimers isolated directly from Alzheimer’s brains impair synaptic plasticity and memory", Nat Med, 14, pp.837~842 (2008)
49. Snyder EM, "Regulation of NMDA receptor trafficking by amyloid-beta", Nat Neurosci, 8, pp.1051~1058 (2005)
50. Chen QS, "Alzheimer amyloid beta-peptide inhibits the late phase of long-term potentiation through calcineurin-dependent mechanisms in the hippocampal dentate gyrus", Neurobiol Learn Mem, 200(77), pp.354~371
51. Shahani N, "Functions and malfunctions of the tau proteins", Cell Mol Life Sci, 59, pp.1668~1680 (2002)
52. Santacruz K, "Tau suppression in a neurodegenerative mouse model improves memory function", Science, 309, pp.476~481 (2005)
53. Oddo S, "Reduction of soluble Abeta and tau, but not soluble Abeta alone, ameliorates cognitive decline in transgenic mice with plaques and tangles", J Biol Chem, 281, pp.39413~39423 (2006)
54. Roberson ED, "Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer’s disease mouse model", Science, 316, pp.750~754 (2007)
55. Rapoport M, "Tau is essential to beta -amyloid-induced neurotoxicity", Proc Natl Acad Sci U S A, 99, pp.6364~6369 (2002)
56. Oddo S, "Abeta immunotherapy leads to clearance of early, but not late, hyperphosphorylated tau aggregates via the proteasome", Neuron, 43, pp.321~332 (2004)
57. Lewis J, "Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP", Science, 293, pp.1487~1491 (2001)
58. Iqbal K, "Tau pathology in Alzheimer disease and other tauopathies", Biochim Biophys Acta, 1739, pp.198~210 (2005)
59. Gong CX, "Post-translational modifications of tau protein in Alzheimer’s disease", J Neural Transm, 112, pp.813~838 (2005)
60. Ittner LM, "Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer’s disease mouse models", Cell, 142, pp.387~397 (2010)
61. Dickey CA, "HSP induction mediates selective clea-rance of tau phosphorylated at proline-directed Ser", Thr sites but not KXGS(MARK)sites, 2006, pp.20, 753~755
62. Myers AJ, "The H1c haplotype at the MAPT locus is associated with Alzheimer’s disease", Hum Mol Genet, 14, pp.2399~2404 (2005)
63. Palop JJ, "Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer’s disease", Neuron, 55, pp.697~711 (2007)
64. Palop JJ, "Epilepsy and cognitive impairments in Alzheimer disease", Arch Neurol, 66, pp.435~440 (2009)
65. Minkeviciene R, "Amyloid beta-induced neuronal hyperexcitability triggers progressive epilepsy", J Neurosci, 29, pp.3453~3462 (2009)
66. Aarts M, "Treatment of ischemic brain damage by perturbing NMDA receptor- PSD-95 protein interactions", Science, 298, pp.846~850 (2002)
67. Nakazawa T, "Regulation of NMDA receptor function by Fyn-mediated tyrosine phosphorylation", Nihon Shinkei Seishin Yakurigaku Zasshi, 22, pp.165~167 (2002)
68. Rong Y, "Tyrosine phosphorylation of ionotropic glutamate receptors by Fyn or Src differentially modulates their susceptibility to calpain and enhances their binding to spectrin and PSD-95", J Neurochem, 79, pp.382~390 (2001)
69. Tezuka T, "PSD-95 promotes Fyn-mediated tyrosine phosphorylation of the N-methyl-D-aspartate receptor subunit NR2A", Proc Natl Acad Sci U S A, 96, pp.435~440 (1999)
70. Chin J, "Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer’s disease", J Neurosci, 25, pp.9694~9703 (2005)
71. Chin J, "Fyn kinase modulates synaptotoxicity, but not aberrant sprouting, in human amyloid precursor protein transgenic mice", J Neurosci, 24, pp.4692~4697 (2004)
72. Baskys A, "Metabotropic receptors and ‘slow’ excitatory actions of glutamate agonists in the hippocampus", Trends Neurosci, 15, pp.92~96 (1992)
73. Nakanishi S, "Molecular diversity of glutamate receptors and implications for brain function", Science, 258, pp.597~603 (1992)
74. Pin JP, "The metabotropic glutamate receptors: structure and functions", Neuropharmacology, 34, pp.1~26 (1995)
75. Bellone C, "Mechanisms of synaptic depression triggered by metabotropic glutamate receptors", Cell Mol Life Sci, 65, pp.2913~2923 (2008)
76. Collingridge GL, "Long-term depression in the CNS", Rev Neurosci, 11, pp.459~473 (2010)
77. Benarroch EE, "Metabotropic glutamate receptors: synaptic modulators and therapeutic targets for neurologic disease", Neurology, 70, pp.964~968 (2008)
78. Wang Q, "Block of long-term potentiation by naturally secreted and synthetic amyloid beta-peptide in hippocampal slices is mediated via activation of the kinases c-Jun N-terminal kinase, cyclin-dependent kinase 5, and p38 mitogen-activated protein kinase as well as metabotropic glutamate receptor type 5", J Neurosci, 24, pp.3370~3378 (2004)
79. Lacor PN, "Synaptic targeting by Alzheimer’srelated amyloid beta oligomers", J Neurosci, 24, pp.10191~10200 (2004)
80. Waung MW, "Rapid translation of Arc", Arg3.1 selectively mediates mGluR-dependent LTD through persistent increases in AMPAR endocytosis rate, 2008, pp.59, 84~97
81. Bruno V, "Activation of metabotropic glutamate receptors coupled to inositol phospholipid hydrolysis amplifies NMDA-induced neuronal degeneration in cultured cortical cells", Neuropharmacology, 34, pp.1089~1098 (1995)
82. Renner M, "Deleterious effects of amyloid beta oligomers acting as an extracellular scaffold for mGlu-R5", Neuron, 66, pp.739~754 (2010)
83. Thathiah A, "G protein-coupled receptors, cholinergic dysfunction, and Abeta toxicity in Alzheimer’s disease", Sci Signal, 2 (2009)
84. Xu X, "Gamma-secretase catalyzes sequential cleavages of the AbetaPP transmembrane domain", J Alzheimers Dis, 16, pp.211~224 (2009)
85. He G, "Gamma-secretase activating protein is a therapeutic target for Alzheimer’s disease", Nature, 467, pp.95~98 (2010)
86. Ghosh AK, "beta-Secretase as a therapeutic target for Alzheimer’s disease", Neurotherapeutics, 5, pp.399~408 (2008)
87. 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)
88. de la Monte SM, "Therapeutic rescue of neurodegeneration in experimental type 3 diabetes: relevance to Alzheimer’s disease", J Alzheimers Dis, 10, pp.89~109 (2006)
89. Akiyama H, "Inflammation and Alzheimer’s disease", Neurobiol Aging, 21, pp.383~421 (2000)
90. Lleo´ A, "Nonsteroidal anti-inflammatory drugs lower Abeta42 and change presenilin 1 conformation", Nat Med, 10, pp.1065~1066 (2004)

관련 논문AI추천