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Synaptic Amyloid-β Oligomers Precede p-Tau and Differentiate High Pathology Control Cases

Bilousova, Tina, Miller, Carol A., Poon, Wayne W., Vinters, Harry V., Corrada, Maria, Kawas, Claudia, Hayden, Eric Y., Teplow, David B., Glabe, Charles, Albay, Ricardo, Cole, Gregory M., Teng, Edmond, Gylys, Karen H.·2016·The American Journal of Pathology

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  1. Larson, 2012, Soluble Abeta oligomer production and toxicity, J Neurochem, 120 Suppl 1, 125, 10.1111/j.1471-4159.2011.07478.x · DOI · Paper page
  2. Hefti, 2013, The case for soluble Abeta oligomers as a drug target in Alzheimer's disease, Trends Pharmacol Sci, 34, 261, 10.1016/j.tips.2013.03.002 · DOI
  3. Giannakopoulos, 2003, Tangle and neuron numbers, but not amyloid load, predict cognitive status in Alzheimer's disease, Neurology, 60, 1495, 10.1212/01.WNL.0000063311.58879.01 · DOI · Paper page
  4. Hyman, 1993, The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution, J Neuropathol Exp Neurol, 52, 594, 10.1097/00005072-199311000-00006 · DOI
  5. Ingelsson, 2004, Early Abeta accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain, Neurology, 62, 925, 10.1212/01.WNL.0000115115.98960.37 · DOI · Paper page
  6. Cummings, 1995, Image analysis of beta-amyloid load in Alzheimer's disease and relation to dementia severity, Lancet, 346, 1524, 10.1016/S0140-6736(95)92053-6 · DOI
  7. Defigueiredo, 1995, Color image analysis in neuroanatomical research: application to senile plaque subtype quantification in Alzheimer's disease, Neurobiol Aging, 16, 211, 10.1016/0197-4580(94)00151-0 · DOI
  8. Kanne, 1998, Relating anatomy to function in Alzheimer's disease: neuropsychological profiles predict regional neuropathology 5 years later, Neurology, 50, 979, 10.1212/WNL.50.4.979 · DOI
  9. Selkoe, 2008, Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior, Behav Brain Res, 192, 106, 10.1016/j.bbr.2008.02.016 · DOI · Paper page
  10. Mairet-Coello, 2013, The CAMKK2-AMPK kinase pathway mediates the synaptotoxic effects of Abeta oligomers through Tau phosphorylation, Neuron, 78, 94, 10.1016/j.neuron.2013.02.003 · DOI · Paper page
  11. Gotz, 2001, Formation of neurofibrillary tangles in P301l tau transgenic mice induced by Abeta 42 fibrils, Science, 293, 1491, 10.1126/science.1062097 · DOI · Paper page
  12. Chabrier, 2012, Soluble abeta promotes wild-type tau pathology in vivo, J Neurosci, 32, 17345, 10.1523/JNEUROSCI.0172-12.2012 · DOI · Paper page
  13. Ittner, 2010, Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models, Cell, 142, 387, 10.1016/j.cell.2010.06.036 · DOI · Paper page
  14. DeKosky, 1996, Structural correlates of cognition in dementia: quantification and assessment of synapse change, Neurodegeneration, 5, 417, 10.1006/neur.1996.0056 · DOI · Paper page
  15. DeKosky, 1990, Synapse loss in frontal cortex biopsies in Alzheimer's disease: correlation with cognitive severity, Ann Neurol, 27, 457, 10.1002/ana.410270502 · DOI · Paper page
  16. Terry, 1991, Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment, Ann Neurol, 30, 572, 10.1002/ana.410300410 · DOI · Paper page
  17. Takahashi, 2002, Intraneuronal Alzheimer abeta42 accumulates in multivesicular bodies and is associated with synaptic pathology, Am J Pathol, 161, 1869, 10.1016/S0002-9440(10)64463-X · DOI · Paper page
  18. Ma, 2012, Amyloid beta: linking synaptic plasticity failure to memory disruption in Alzheimer's disease, J Neurochem, 120 Suppl 1, 140, 10.1111/j.1471-4159.2011.07506.x · DOI
  19. Cirrito, 2005, Synaptic activity regulates interstitial fluid amyloid-beta levels in vivo, Neuron, 48, 913, 10.1016/j.neuron.2005.10.028 · DOI · Paper page
  20. Sokolow, 2012, AD synapses contain abundant Abeta monomer and multiple soluble oligomers, including a 56-kDa assembly, Neurobiol Aging, 33, 1545, 10.1016/j.neurobiolaging.2011.05.011 · DOI
  21. Henkins, 2012, Extensive p-tau pathology and SDS-stable p-tau oligomers in Alzheimer's cortical synapses, Brain Pathol, 22, 826, 10.1111/j.1750-3639.2012.00598.x · DOI
  22. Tai, 2012, The synaptic accumulation of hyperphosphorylated tau oligomers in Alzheimer disease is associated with dysfunction of the ubiquitin-proteasome system, Am J Pathol, 181, 1426, 10.1016/j.ajpath.2012.06.033 · DOI · Paper page
  23. Maeda, 2006, Increased levels of granular tau oligomers: an early sign of brain aging and Alzheimer's disease, Neurosci Res, 54, 197, 10.1016/j.neures.2005.11.009 · DOI · Paper page
  24. Patterson, 2011, Characterization of prefibrillar Tau oligomers in vitro and in Alzheimer disease, J Biol Chem, 286, 23063, 10.1074/jbc.M111.237974 · DOI
  25. Yang, 1994, Monoclonal antibody to the C-terminus of beta-amyloid, Neuroreport, 5, 2117, 10.1097/00001756-199410270-00032 · DOI
  26. Fein, 2008, Co-localization of amyloid beta and tau pathology in Alzheimer's disease synaptosomes, Am J Pathol, 172, 1683, 10.2353/ajpath.2008.070829 · DOI
  27. Flood, 2009, A transgenic rat model of Alzheimer's disease with extracellular Abeta deposition, Neurobiol Aging, 30, 1078, 10.1016/j.neurobiolaging.2007.10.006 · DOI
  28. Teng, 2011, [F-18]FDDNP microPET imaging correlates with brain Abeta burden in a transgenic rat model of Alzheimer disease: effects of aging, in vivo blockade, and anti-Abeta antibody treatment, Neurobiol Dis, 43, 565, 10.1016/j.nbd.2011.05.003 · DOI
  29. Liu, 2008, A transgenic rat that develops Alzheimer's disease-like amyloid pathology, deficits in synaptic plasticity and cognitive impairment, Neurobiol Dis, 31, 46, 10.1016/j.nbd.2008.03.005 · DOI
  30. Gylys, 2004, Enrichment of presynaptic and postsynaptic markers by size-based gating analysis of synaptosome preparations from rat and human cortex, Cytometry A, 60, 90, 10.1002/cyto.a.20031 · DOI
  31. Rosensweig, 2012, Preparation of stable amyloid beta-protein oligomers of defined assembly order, Methods Mol Biol, 849, 23, 10.1007/978-1-61779-551-0_3 · DOI
  32. Lim, 2000, Ibuprofen suppresses plaque pathology and inflammation in a mouse model for Alzheimer's disease, J Neurosci, 20, 5709, 10.1523/JNEUROSCI.20-15-05709.2000 · DOI
  33. Dunkley, 2008, A rapid Percoll gradient procedure for preparation of synaptosomes, Nat Protoc, 3, 1718, 10.1038/nprot.2008.171 · DOI
  34. Wilhelm, 2014, Composition of isolated synaptic boutons reveals the amounts of vesicle trafficking proteins, Science, 344, 1023, 10.1126/science.1252884 · DOI · Paper page
  35. Gylys, 2007, Increased cholesterol in Abeta-positive nerve terminals from Alzheimer's disease cortex, Neurobiol Aging, 28, 8, 10.1016/j.neurobiolaging.2005.10.018 · DOI
  36. Gylys, 2003, Apolipoprotein E enhances uptake of soluble but not aggregated amyloid-beta protein into synaptic terminals, J Neurochem, 84, 1442, 10.1046/j.1471-4159.2003.01643.x · DOI · Paper page
  37. Sokolow, 2012, Isolation of synaptic terminals from Alzheimer's disease cortex, Cytometry A, 81, 248, 10.1002/cyto.a.22009 · DOI
  38. Hatami, 2014, Monoclonal antibodies against Abeta42 fibrils distinguish multiple aggregation state polymorphisms in vitro and in Alzheimer disease brain, J Biol Chem, 289, 32131, 10.1074/jbc.M114.594846 · DOI
  39. Gylys, 2004, Synaptic changes in Alzheimer's disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence, Am J Pathol, 165, 1809, 10.1016/S0002-9440(10)63436-0 · DOI · Paper page
  40. Thal, 2002, Phases of A beta-deposition in the human brain and its relevance for the development of AD, Neurology, 58, 1791, 10.1212/WNL.58.12.1791 · DOI · Paper page
  41. Bernstein, 2009, Amyloid-beta protein oligomerization and the importance of tetramers and dodecamers in the aetiology of Alzheimer's disease, Nat Chem, 1, 326, 10.1038/nchem.247 · DOI
  42. Lesne, 2013, Brain amyloid-beta oligomers in ageing and Alzheimer's disease, Brain, 136, 1383, 10.1093/brain/awt062 · DOI
  43. Esparza, 2013, Amyloid-beta oligomerization in Alzheimer dementia versus high-pathology controls, Ann Neurol, 73, 104, 10.1002/ana.23748 · DOI
  44. Bruggink, 2013, Amyloid-beta oligomer detection by ELISA in cerebrospinal fluid and brain tissue, Anal Biochem, 433, 112, 10.1016/j.ab.2012.09.014 · DOI
  45. Kasai, 2013, Correlation of Abeta oligomer levels in matched cerebrospinal fluid and serum samples, Neurosci Lett, 551, 17, 10.1016/j.neulet.2013.06.029 · DOI
  46. Yang, 2013, New ELISAs with high specificity for soluble oligomers of amyloid beta-protein detect natural Abeta oligomers in human brain but not CSF, Alzheimers Dement, 9, 99, 10.1016/j.jalz.2012.11.005 · DOI
  47. McLean, 2013, Positron emission tomography imaging of fibrillar parenchymal and vascular amyloid-beta in TgCRND8 mice, ACS Chem Neurosci, 4, 613, 10.1021/cn300226q · DOI
  48. Kayed, 2010, Conformation dependent monoclonal antibodies distinguish different replicating strains or conformers of prefibrillar Abeta oligomers, Mol Neurodegener, 5, 57, 10.1186/1750-1326-5-57 · DOI
  49. Kopeikina, 2013, Synaptic alterations in the rTg4510 mouse model of tauopathy, J Comp Neurol, 521, 1334, 10.1002/cne.23234 · DOI
  50. Pooler, 2013, Tau-amyloid interactions in the rTgTauEC model of early Alzheimer's disease suggest amyloid-induced disruption of axonal projections and exacerbated axonal pathology, J Comp Neurol, 521, 4236, 10.1002/cne.23411 · DOI
  51. Moechars, 1999, Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain, J Biol Chem, 274, 6483, 10.1074/jbc.274.10.6483 · DOI · Paper page
  52. Aizenstein, 2008, Frequent amyloid deposition without significant cognitive impairment among the elderly, Arch Neurol, 65, 1509, 10.1001/archneur.65.11.1509 · DOI · Paper page
  53. Mintun, 2006, [11C]PIB in a nondemented population: potential antecedent marker of Alzheimer disease, Neurology, 67, 446, 10.1212/01.wnl.0000228230.26044.a4 · DOI · Paper page
  54. Gouras, 2012, Critical role of intraneuronal Abeta in Alzheimer's disease: technical challenges in studying intracellular Abeta, Life Sci, 91, 1153, 10.1016/j.lfs.2012.06.004 · DOI · Paper page
  55. Cirrito, 2008, Endocytosis is required for synaptic activity-dependent release of amyloid-beta in vivo, Neuron, 58, 42, 10.1016/j.neuron.2008.02.003 · DOI · Paper page
  56. Bero, 2011, Neuronal activity regulates the regional vulnerability to amyloid-beta deposition, Nat Neurosci, 14, 750, 10.1038/nn.2801 · DOI · Paper page
  57. Yang, 2011, Reversal of autophagy dysfunction in the TgCRND8 mouse model of Alzheimer's disease ameliorates amyloid pathologies and memory deficits, Brain, 134, 258, 10.1093/brain/awq341 · DOI · Paper page
  58. Cataldo, 1996, Properties of the endosomal-lysosomal system in the human central nervous system: disturbances mark most neurons in populations at risk to degenerate in Alzheimer's disease, J Neurosci, 16, 186, 10.1523/JNEUROSCI.16-01-00186.1996 · DOI
  59. Bennett, 2014, Cognitive and social lifestyle: links with neuropathology and cognition in late life, Acta Neuropathol, 127, 137, 10.1007/s00401-013-1226-2 · DOI
  60. Bjorklund, 2012, Absence of amyloid beta oligomers at the postsynapse and regulated synaptic Zn2+ in cognitively intact aged individuals with Alzheimer's disease neuropathology, Mol Neurodegener, 7, 23, 10.1186/1750-1326-7-23 · DOI · Paper page
  61. Koffie, 2009, Oligomeric amyloid beta associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques, Proc Natl Acad Sci U S A, 106, 4012, 10.1073/pnas.0811698106 · DOI · Paper page
  62. Braak, 1995, Staging of Alzheimer's disease-related neurofibrillary changes, Neurobiol Aging, 16, 271, 10.1016/0197-4580(95)00021-6 · DOI · Paper page
  63. Dujardin, 2014, Neuron-to-neuron wild-type Tau protein transfer through a trans-synaptic mechanism: relevance to sporadic tauopathies, Acta Neuropathol Commun, 2, 14, 10.1186/2051-5960-2-14 · DOI
  64. Jin, 2011, Soluble amyloid beta-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration, Proc Natl Acad Sci U S A, 108, 5819, 10.1073/pnas.1017033108 · DOI · Paper page
  65. Walker, 2013, Mechanisms of protein seeding in neurodegenerative diseases, JAMA Neurol, 70, 304, 10.1001/jamaneurol.2013.1453 · DOI · Paper page
  66. Ittner, 2011, Amyloid-beta and tau–a toxic pas de deux in Alzheimer's disease, Nat Rev Neurosci, 12, 65, 10.1038/nrn2967 · DOI · Paper page
  67. Hernandez, 2014, Research tool: validation of floxed alpha7 nicotinic acetylcholine receptor conditional knockout mice using in vitro and in vivo approaches, J Physiol, 592, 3201, 10.1113/jphysiol.2014.272054 · DOI

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Metadata

Authors
Bilousova, T., Miller, C. A., Poon, W. W., Vinters, H. V., Corrada, M., Kawas, C., Hayden, E. Y., Teplow, D. B., Glabe, C., Albay, R., Cole, G. M., Teng, E., & Gylys, K. H.
Venue
The American Journal of Pathology
Publisher
Elsevier BV
Published
2016-01
Volume
186
Issue
1
Pages
185-198
ISSN
0002-9440
Cited by
115
References
20
Language
en
Funders
  • NIH (AG27465, NS038328, AG041295, CA16042, AI 28697)
  • National Institute on Aging (AG18879, AG34628, UL1TR000124)
  • University of California Los Angeles Clinical and Translational Science Institute
  • UCLA Older Americans Independence Center (P30 AG028748)
  • NIA (R01AG21055)

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