Alzheimer's Disease and Amyloid: Culprit or Coincidence?

International Review of Neurobiology

Volumn 102, Issue , 2012, Pages 277-316

  Skaper, Stephen D ^a  

^a UNIVERSITY OF PADOVA   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA TOCOPHEROL; AMINO ACID; AMYLOID BETA PROTEIN; AMYLOID BETA PROTEIN[1-40]; AMYLOID BETA PROTEIN[1-42]; AMYLOID PRECURSOR PROTEIN; AMYLOID PROTEIN; ANTIINFLAMMATORY AGENT; APOLIPOPROTEIN E4; MITOCHONDRIAL DNA; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; PLACEBO; REACTIVE OXYGEN METABOLITE; TAU PROTEIN;

ALZHEIMER DISEASE; AMYLOID PLAQUE; ARTICLE; BIOACCUMULATION; DISEASE COURSE; DNA DAMAGE; HUMAN; IMMUNOTHERAPY; MUTATION; NERVE CELL DEGENERATION; NERVOUS SYSTEM INFLAMMATION; NEUROFIBRILLARY TANGLE; NEUROPROTECTION; NONHUMAN; OXIDATIVE STRESS; PATHOGENESIS; PATHOPHYSIOLOGY; PEPTIDE SYNTHESIS; PRIORITY JOURNAL; PROTEIN DEFECT; PROTEIN EXPRESSION; PROTEIN LOCALIZATION; PROTEIN PROCESSING; SENILE PLAQUE; SYMPTOM; SYNAPSE; TRANSGENIC ANIMAL; WHITE MATTER;

EID: 84862842525     PISSN: 00747742     EISSN: None     Source Type: Book Series    
DOI: 10.1016/B978-0-12-386986-9.00011-9     Document Type: Chapter

References (265)

1. Allen B., Ingram E., Takao M., Smith M.J., Jakes R., Virdee K., Yoshida H., Holzer M., Craxton M., Emson P.C., Atzori C., Migheli A., et al. Abundant tau filaments and nonapoptotic neurodegeneration in transgenic mice expressing human P301S tau protein. J. Neurosci. 2002, 22(21):9340-9351.
2. Alzheimer's Association 2009 Alzheimer's disease facts and figures. Alzheimers Dement. 2009, 5:234-270.
3. Amniai L., Barbier P., Sillen A., Wieruszeski J.M., Peyrot V., Lippens G., Landrieu I. Alzheimer disease specific phosphoepitopes of tau interfere with assembly of tubulin but not binding to microtubules. FASEB J. 2009, 23(4):1146-1152.
4. Anandatheerthavarada H.K., Biswas G., Robin M.A., Avadhani N.G. Mitochondrial targeting and a novel transmembrane arrest of Alzheimer's amyloid precursor protein impairs mitochondrial function in neuronal cells. J. Cell Biol. 2003, 161(1):41-54.
5. Andorfer C., Acker C.M., Kress Y., Hof P.R., Duff K., Davies P. Cell-cycle reentry and cell death in transgenic mice expressing nonmutant human tau isoforms. J. Neurosci. 2005, 25(22):5446-5454.
6. Andreyev A.Y., Kushnareva Y.E., Starkov A.A. Mitochondrial metabolism of reactive oxygen species. Biochemistry (Mosc.) 2005, 70(2):200-214.
7. Balaban R.S., Nemoto S., Funkel T. Mitochondria, oxidants, and aging. Cell 2005, 120(4):483-495.
8. Bartzokis G. Alzheimer's disease as homeostatic responses to age-related myelin breakdown. Neurobiol. Aging 2011, 32(8):1341-1371. (Review).
9. Benfenati F., Valtorta F., Bähler M., Greengard P. Synapsin I, a neuron-specific phosphoprotein interacting with small synaptic vesicles and F-actin. Cell Biol. Int. Rep. 1989, 13(12):1007-1021. Review.
10. Bentahir M., Nyabi O., Verhamme J., Tolia A., Horré K., Wiltfang J., Esselmann H., De Strooper B. Presenilin clinical mutations can affect γ-secretase activity by different mechanisms. J. Neurochem. 2006, 96(3):732-742.
11. Bertram L., Tanzi R.E. The genetic epidemiology of neurodegenerative disease. J. Clin. Invest. 2005, 115(6):1449-1457. (Review).
12. Billings L.M., Oddo S., Green K.N., McGaugh J.L., LaFerla F.M. Intraneuronal Aβ causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice. Neuron 2005, 45(5):675-688.
13. Billingsley M.L., Kincaid R.L. Regulated phosphorylation and dephosphorylation of tau protein: effects on microtubule interaction, intracellular trafficking and neurodegeneration. Biochem. J. 1997, 323(Pt 3):577-591.
14. Block M.L., Zecca L., Hong J.S. Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. Nat. Rev. Neurosci. 2007, 8(1):57-69.
15. Borchelt D.R., Ratovitski T., van Lare J., Lee M.K., Gonzales V., Jenkins N.A., Copeland N.G., Price D.L., Sisodia S.S. Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins. Neuron 1997, 19(4):939-945.
16. Braak H., Braak E. Development of Alzheimer-related neurofibrillary changes in the neocortex inversely recapitulates cortical myelogenesis. Acta Neuropathol. 1996, 92(2):197-201.
17. Brun A., Englund E. A white matter disorder in dementia of the Alzheimer type: a pathoanatomical study. Ann. Neurol. 1986, 19(3):253-262.
18. Buckner R.L., Snyder A.Z., Shannon B.L., LaRossa G., Sachs R., Fotenos A.F., Sheline Y.I., Klunk W.E., Mathis C.A., Morris J.C., Mintun M.A. Molecular, structural, and functional characterization of Alzheimer's disease: evidence for a relationship between default activity, amyloid, and memory. J. Neurosci. 2005, 25(34):7709-7717.
19. Busciglio J., Pelsman A., Wong C., Pigino G., Yuan M., Mori H., Yankner B.A. Altered metabolism of the amyloid β precursor protein is associated with mitochondrial dysfunction in Down's syndrome. Neuron 2002, 33(5):677-688.
20. Buxbaum J.D., Thinakaran G., Koliatsos V., O'Callahan J., Slunt H.H., Price D.L., Sisodia S.S. Alzheimer amyloid protein precursor in the rat hippocampus: transport and processing through the perforant path. J. Neurosci. 1998, 18(23):9629-9637.
21. Capsoni S., Tiveron C., Vignone D., Amato G., Cattaneo A. Dissecting the involvement of tropomyosin-related kinase A and p75 neurotrophin receptor signaling in NGF deficit-induced neurodegeneration. Proc. Natl. Acad. Sci. USA 2010, 107(27):12299-12304.
22. Capsoni S., Brandi R., Arisi I., D'Onofrio M., Cattaneo A. A dual mechanism linking NGF/proNGF imbalance and early inflammation to Alzheimer's disease neurodegeneration in the AD11 anti-NGF mouse model. CNS Neurol. Disord. Drug Targets 2011, 10(5):635-647. (Review).
23. Cash A.D., Aliev G., Siedlak S.L., Nunomura A., Fujioka H., Zhu X., Raina A.K., Vinters H.V., Tabaton M., Johnson A.B., Paula-Barbosa M., Avíla J., et al. Microtubule reduction in Alzheimer's disease and aging is independent of tau filament formation. Am. J. Pathol. 2003, 162(5):1623-1627.
24. Casley C.S., Canevari L., Land J.M., Clark J.B., Sharpe M.A. β-amyloid inhibits integrated mitochondrial respiration and key enzyme activities. J. Neurochem. 2002, 80(1):91-100.
25. Cataldo A.M., Peterhoff C.M., Troncoso J.C., Gomez-Isla T., Hyman B.T., Nixon R.A. Endocytic pathway abnormalities precede amyloid β deposition in sporadic Alzheimer's disease and Down syndrome: differential effects of APOE genotype and presenilin mutations. Am. J. Pathol. 2000, 157(1):277-286.
26. Cattaneo A., Capsoni S., Paoletti F. Towards non invasive nerve growth factor therapies for Alzheimer's disease. J. Alzheimers Dis. 2008, 15(2):255-283. (Review).
27. Chen Q.S., Wei W.Z., Shimahara T., Xie C.W. Alzheimer amyloid β-peptide inhibits the late phase of long-term potentiation through calcineurin-dependent mechanisms in the hippocampal dentate gyrus. Neurobiol. Learn. Mem. 2002, 77(3):354-371.
28. Chin L., Li L., Ferreira A., Kosik K.S., Greengard P. Impairment of axonal development and of synaptogenesis in hippocampal neurons of synapsin I-deficient mice. Proc. Natl. Acad. Sci. USA 1995, 92(20):9230-9234.
29. Chishti M.A., Yang D.S., Janus C., Phinney A.L., Horne P., Pearson J., Strome R., Zuker N., Loukides J., French J., Turner S., Lozza G., et al. Early-onset amyloid deposition and cognitive deficits in transgenic mice expressing a double mutant form of amyloid precursor protein 695. J. Biol. Chem. 2001, 276(24):21562-21570.
30. Cirrito J.R., Yamada K.A., Finn M.B., Sloviter R.S., Bales K.R., May P.C., Schoepp D.D., Paul S.M., Mennerick S., Holtzman D.M. Synaptic activity regulates interstitial fluid amyloid-β levels in vivo. Neuron 2005, 48(6):913-922.
31. Citron M. Alzheimer's disease: strategies for disease modification. Nat. Rev. Drug Discov. 2010, 9(5):387-398.
32. Corral-Debrinski M., Horton T., Lott M.T., Shoffner J.M., Beal M.F., Wallace D.C. Mitochondrial DNA deletions in human brain: regional variability and increase with advanced age. Nat. Genet. 1992, 2(4):324-329.
33. Coskun P.E., Beal M.F., Wallace D.C. Alzheimer's brains harbor somatic mtDNA control-region mutations that suppress mitochondrial transcription and replication. Proc. Natl. Acad. Sci. USA 2004, 101(29):10726-10731.
34. Craft J.M., Watterson D.M., Van Eldik L.J. Neuroinflammation: a potential therapeutic target. Expert Opin. Ther. Targets 2005, 9(5):887-900.
35. Crews L., Patrick C., Adame A., Rockenstein E., Masliah E. Modulation of aberrant CDK5 signaling rescues impaired neurogenesis in models of Alzheimer's disease. Cell Death Dis. 2011, 2:e120. Published online 10 February 2011. 10.1038/cddis.2011.2.
36. Crouch P.J., Blake R., Duce J.A., Ciccotosto G.D., Li Q.X., Barnham K.J., Curtain C.C., Cherny R.A., Cappai R., Dyrks T., Masters C.L., Trounce I.A. Copper-dependent inhibition of human cytochrome c oxidase by a dimeric conformer of amyloid-β1-42. J. Neurosci. 2005, 25(3):672-679.
37. Cuchillo-Ibanez I., Seereeram A., Byers H.L., Leung K.Y., Ward M.A., Anderton B.H., Hanger D.P. Phosphorylation of tau regulates its axonal transport by controlling its binding to kinesin. FASEB J. 2008, 22(9):3186-3195.
38. Cuello A.C., Bruno M.A. The failure in NGF maturation and its increased degradation as the probable cause for the vulnerability of cholinergic neurons in Alzheimer's disease. Neurochem. Res. 2007, 32(6):1041-1045. (Review).
39. Davies C.A., Mann D.M., Sumpter P.Q., Yates P.O. A quantitative morphometric analysis of the neuronal and synaptic content of the frontal and temporal cortex in patients with Alzheimer's disease. J. Neurol. Sci. 1987, 78(2):151-164.
40. De Felice F.G., Velasco P.T., Lambert M.P., Viola K., Fernandez S.J., Ferreira S.T., Klein W.L. Aβ oligomers induce neuronal oxidative stress through an N-methyl-d-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine. J. Biol. Chem. 2007, 282(15):11590-11601.
41. De Felice F.G., Wu D., Lambert M.P., Fernandez S.J., Velasco P.T., Lacor P.N., Bigio E.H., Jerecic J., Acton P.J., Shughrue P.J., Chen-Dodson E., Kinney G.G., et al. Alzheimer's disease-type neuronal tau hyperphosphorylation induced by Aβ oligomers. Neurobiol. Aging 2008, 29(9):1334-1347.
42. Decker H., Lo K.Y., Unger S.M., Ferreira S.T., Silverman M.A. Amyloid-β peptide oligomers disrupt axonal transport through an NMDA receptor-dependent mechanism that is mediated by glycogen synthase kinase 3β in primary cultured hippocampal neurons. J. Neurosci. 2010, 30(27):9166-9171.
43. DeKosky S.T., Scheff S.W. Synapse loss in frontal cortex biopsies in Alzheimer's disease: correlation with cognitive severity. Ann. Neurol. 1990, 27(5):457-464.
44. Dermaut B., Kumar-Singh S., Engelborghs S., Theuns J., Rademakers R., Saerens J., Pickut B.A., Peeters K., van den Broeck M., Vennekens K., Claes S., Cruts M., et al. A novel presenilin 1 mutation associated with Pick's disease but not β-amyloid plaques. Ann. Neurol. 2004, 55(5):617-626.
45. Desai M.K., Sudol K.L., Janelsins M.C., Mastrangelo M.A., Frazer M.E., Bowers W.J. Triple-transgenic Alzheimer's disease mice exhibit region-specific abnormalities in brain myelination patterns prior to appearance of amyloid and tau pathology. Glia 2009, 57(1):54-65.
46. Desai M.K., Guercio B.J., Narrow W.C., Bowers W.J. An Alzheimer's disease-relevant presenilin-1 mutation augments amyloid-beta-induced oligodendrocyte dysfunction. Glia 2011, 59(4):627-640.
47. Dewachter I., Filipkowski R.K., Priller C., Ris L., Neyton J., Croes S., Terwel D., Gysemans M., Devijver H., Borghgraef P., Godaux E., Kaczmarek L., et al. Deregulation of NMDA-receptor function and down-stream signaling in APP[V717I] transgenic mice. Neurobiol. Aging 2009, 30(2):241-256.
48. Dhavan R., Tsai L.H. A decade of CDK5. Nat. Rev. Mol. Cell Biol. 2001, 2(10):749-759. (Review).
49. Dickerson B.C., Sperling R.A. Functional abnormalities of the medial temporal lobe memory system in mild cognitive impairment and Alzheimer's disease: insights from functional MRI studies. Neuropsychologia 2008, 46(6):1624-1635.
50. Dodart J.C., Bales K.R., Gannon K.S., Greene S.J., DeMattos R.B., Mathis C., DeLong C.A., Wu S., Wu X., Holtzman D.M., Paul S.M. Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model. Nat. Neurosci. 2002, 5(5):452-457.
51. Dodel R.C., Du Y., Depboylu C., Hampel H., Frölich L., Haag A., Hemmeter U., Paulsen S., Teipel S.J., Brettschneider S., Spottke A., Nölker C., et al. Intravenous immunoglobulins containing antibodies against β-amyloid for the treatment of Alzheimer's disease. J. Neurol. Neurosurg. Psychiatry 2004, 75(10):1472-1474.
52. Dodel R., Balakrishnan K., Keyvani K., Deuster O., Neff F., Andrei-Selmer L.-C., Röskam S., Stüer C., Al-Abed Y., Noelker C., Balzer-Geldsetzer M., Oertel W., et al. Naturally occurring autoantibodies against β-amyloid: investigating their role in transgenic animal and in vitro models of Alzheimer's disease. J. Neurosci. 2011, 31(15):5847-5854.
53. Du Y., Dodel R., Hampel H., Buerger K., Lin S., Eastwood B., Bales K., Gao F., Moeller H.J., Oertel W., Farlow M., Paul S. Reduced levels of amyloid β-peptide antibody in Alzheimer disease. Neurology 2001, 57(5):801-805.
54. Dubois B., Feldman H.H., Jacova C., Dekosky S.T., Barberger-Gateau P., Cummings J., Delacourte A., Galasko D., Gauthier S., Jicha G., Meguro K., O'Brien J., et al. Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS-ADRDA criteria. Lancet Neurol. 2007, 8:734-746. (Review).
55. Dumont M., Wille E., Stack C., Calingasan N.Y., Beal M.F., Lin M.T. Reduction of oxidative stress, amyloid deposition, and memory deficit by manganese superoxide dismutase overexpression in a transgenic mouse model of Alzheimer's disease. FASEB J. 2009, 23(8):2459-2466.
56. Eckert A., Schmitt K., Götzm J. Mitochondrial dysfunction-the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicity. Alzheimers Res. Ther. 2011, 3(2):15.
57. Edison P., Archer H.A., Hinz R., Hammers A., Pavese N., Tai Y.F., Hotton G., Cutler D., Fox N., Kennedy A., Rossor M., Brooks D.J. Amyloid, hypometabolism, and cognition in Alzheimer disease: an [11C]PIB and [18F]FDG PET study. Neurology 2007, 68(7):501-508.
58. El Khoury J., Luster A.D. Mechanisms of microglia accumulation in Alzheimer's disease: therapeutic implications. Trends Pharmacol. Sci. 2008, 29(12):626-632. (Review).
59. Elson J.L., Herrnstadt C., Preston G., Thal L., Morris C.M., Edwardson J.A., Beal M.F., Turnbull D.M., Howell N. Does the mitochondrial genome play a role in the etiology of Alzheimer's disease?. Hum. Genet. 2006, 119(3):241-254.
60. Engmann O., Giese K.P. Crosstalk between Cdk5 and GSK3β: implications for Alzheimer's disease. Front. Mol. Neurosci. 2009, 2:2. Review. 10.3389/neuro.02.002.2009.
61. Esposito L., Raber J., Kekonius L., Yan F., Yu G.Q., Bien-Ly N., Puoliväli J., Scearce-Levie K., Masliah E., Mucke L. Reduction in mitochondrial superoxide dismutase modulates Alzheimer's disease-like pathology and accelerates the onset of behavioral changes in human amyloid precursor protein transgenic mice. J. Neurosci. 2006, 26(19):5167-5179.
62. 1-42 reduces synapse number and inhibits neurite outgrowth in primary cortical and hippocampal neurons: a quantitative analysis. J. Neurosci. Methods 2008, 175(1):96-103.
63. Firbank M.J., Blamire A.M., Krishnan M.S., Teodorczuk A., English P., Gholkar A., Harrison R., O'Brien J.T. Atrophy is associated with posterior cingulate white matter disruption in dementia with Lewy bodies and Alzheimer's disease. Neuroimage 2007, 36(1):1-7.
64. Fuhrmann M., Bittner T., Jung C.K., Burgold S., Page R.M., Mitteregger G., Haass C., LaFerla F.M., Kretzschmar H., Herms J. Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease. Nat. Neurosci. 2010, 13(4):411-413.
65. Fukumoto H., Tokuda T., Kasai T., Ishigami N., Hidaka H., Kondo M., Allsop D., Nakagawa M. High-molecular-weight β-amyloid oligomers are elevated in cerebrospinal fluid of Alzheimer patients. FASEB J. 2010, 24(8):2716-2726.
66. Games D., Adams D., Alessandrini R., Barbour R., Berthelette P., Blackwell C., Carr T., Clemens J., Donaldson T., Gillespie F., Guido T., Hagopian S., et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein. Nature 1995, 373(6514):523-527.
67. Gao Y., Pimplikar S.W. The γ-secretase-cleaved C-terminal fragment of amyloid precursor protein mediates signaling to the nucleus. Proc. Natl. Acad. Sci. USA 2001, 98(26):14979-14984.
68. Ghosal K., Vogt D.L., Liang M., Shen Y., Lamb B.T., Pimplikar S.W. Alzheimer's disease-like pathological features in transgenic mice expressing the APP intracellular domain. Proc. Natl. Acad. Sci. USA 2009, 106(43):18367-18372.
69. Gibson G.E., Sheu K.F., Blass J.P., Baker A., Carlson K.C., Harding B., Perrino P. Reduced activities of thiamine-dependent enzymes in the brains and peripheral tissues of patients with Alzheimer's disease. Arch. Neurol. 1988, 45(8):836-840.
70. Ginsberg S.D., Alldred M.J., Counts S.E., Cataldo A.M., Neve R.L., Jiang Y., Wuu J., Chao M.V., Mufson E.J., Nixon R.A., Che S. Microarray analysis of hippocampal CA1 neurons implicates early endosomal dysfunction during Alzheimer's disease progression. Biol. Psychiatry 2010, 68(10):885-893.
71. Glabe C. Intracellular mechanisms of amyloid accumulation and pathogenesis in Alzheimer's disease. J. Mol. Neurosci. 2001, 17(2):137-145. (Review).
72. Glabe C.G. Structural classification of toxic amyloid oligomers. J. Biol. Chem. 2008, 283(44):29639-29643.
73. Glenner G.G., Wong C.W. Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem. Biophys. Res. Commun. 1984, 120(3):885-890.
74. Goedert M., Wischik C.M., Crowther R.A., Walker J.E., Klug A. Cloning and sequencing of the cDNA encoding a core protein of the paired helical filament of Alzheimer disease: identification as the microtubule-associated protein tau. Proc. Natl. Acad. Sci. USA 1988, 85(11):4051-4055.
75. Gonatas N.K., Anderson W., Evangelista I. The contribution of altered synapses in the senile plaque: an electron microscopic study in Alzheimer's dementia. J. Neuropathol. Exp. Neurol. 1967, 26(1):25-39.
76. Götz J., Streffer J.R., David D., Schild A., Hoerndli F., Pennanen L., Kurosinski P., Chen F. Transgenic animal models of Alzheimer's disease and related disorders: histopathology, behavior and therapy. Mol. Psychiatry 2004, 9(7):664-683. (Review).
77. Götz J., Ittner L.M., Kins S. Do axonal defects in tau and amyloid precursor protein transgenic animals model axonopathy in Alzheimer's disease?. J. Neurochem. 2006, 98(4):993-1006.
78. Grathwohl S.A., Kälin R.E., Bolmont T., Prokop S., Winkelmann G., Kaeser S.A., Odenthal J., Radde R., Eldh T., Gandy S., Aguzzi A., Staufenbiel M., et al. Formation and maintenance of Alzheimer's disease β-amyloid plaques in the absence of microglia. Nat. Neurosci. 2009, 12(11):1361-1363.
79. Greenberg S.M., Shin Y., Grabowski T.J., Cooper G.E., Rebeck G.W., Iglesias S., Chapon F., Tournier-Lasserve E., Baron J.C. Hemorrhagic stroke associated with the Iowa amyloid precursor protein mutation. Neurology 2003, 60(6):1020-1022.
80. Grueninger F., Bohrmann B., Czech C., Ballard T.M., Frey J.R., Weidensteiner C., von Kienlin M., Ozmen L. Phosphorylation of Tau at S422 is enhanced by Aβ in TauPS2APP triple transgenic mice. Neurobiol. Dis. 2010, 37(2):294-306.
81. Haass C., Selkoe D.J. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide. Nat. Rev. Mol. Cell Biol. 2007, 8(2):101-112. (Review).
82. Hamos J.E., DeGennaro L.J., Drachman D.A. Synaptic loss in Alzheimer's disease and other dementias. Neurology 1989, 39(3):355-361.
83. Hanger D.P., Byers H.L., Wray S., Leung K.Y., Saxton M.J., Seereeram A., Reynolds C.H., Ward M.A., Anderton B.H. Novel phosphorylation sites in tau from Alzheimer brain support a role for casein kinase 1 in disease pathogenesis. J. Biol. Chem. 2007, 282(32):23645-23654.
84. Hanger D.P., Seereeram A., Noble W. Mediators of tau phosphorylation in the pathogenesis of Alzheimer's disease. Expert Rev. Neurother. 2009, 9(11):1647-1666. (Review).
85. Hanisch U.-K., Kettenmann H. Microglia: active sensor and versatile effector cells in the normal and pathologic brain. Nat. Neurosci. 2007, 10(11):1387-1394.
86. Hansson C.A., Frykman S., Farmery M.R., Tjernberg L.O., Nilsberth C., Pursglove S.E., Ito A., Winblad B., Cowburn R.F., Thyberg J., Ankarcrona M. Nicastrin, presenilin, APH-1, and PEN-2 form active γ-secretase complexes in mitochondria. J. Biol. Chem. 2004, 279(49):51654-51660.
87. Harmeier A., Wozny C., Rost B.R., Munter L.M., Hua H., Georgiev O., Beyermann M., Hildebrand P.W., Weise C., Schaffner W., Schmitz D., Multhaup G. Role of amyloid-β glycine 33 in oligomerization, toxicity, and neuronal plasticity. J. Neurosci. 2009, 29(23):7582-7590.
88. Harms M.P., Kotyk J.J., Merchant K.M. Evaluation of white matter integrity in ex vivo brains of amyloid plaque-bearing APPsw transgenic mice using magnetic resonance diffusion tensor imaging. Exp. Neurol. 2006, 199(2):408-415.
89. Harold D., et al. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease. Nat. Genet. 2009, 41(10):1088-1093.
90. Heneka M.T., Nadrigny F., Regen T., Martinez-Hernandez A., Dumitrescu-Ozimek L., Terwel D., Jardanhazi-Kurutz D., Walter J., Kirchhoff F., Hanisch U.K., Kummer M.P. Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine. Proc. Natl. Acad. Sci. USA 2010, 107(13):6058-6063.
91. Holcomb L., Gordon M.N., McGowan E., Yu X., Benkovic S., Jantzen P., Wright K., Saad I., Mueller R., Morgan D., Sanders S., Zehr C., et al. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes. Nat. Med. 1998, 4(1):97-100.
92. Hoshi M., Sato M., Matsumoto S., Noguchi A., Yasutake K., Yoshida N., Sato K. Spherical aggregates of β-amyloid (amylospheroid) show high neurotoxicity and activate tau protein kinase I/glycogen synthase kinase-3β. Proc. Natl. Acad. Sci. USA 2003, 100(11):6370-6375.
93. Houeland G., Romani A., Marchetti C., Amato G., Capsoni S., Cattaneo A., Marie H. Transgenic mice with chronic NGF deprivation and Alzheimer's disease-like pathology display hippocampal region-specific impairments in short- and long-term plasticities. J. Neurosci. 2010, 30(39):13089-13094.
94. Hsiao K., Chapman P., Nilsen S., Eckman C., Harigaya Y., Younkin S., Yang F., Cole G. Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice. Science 1996, 274(5284):99-102.
95. Hsieh H., Boehm J., Sato C., Iwatsubo T., Tomita T., Sisodia S., Malonow R. AMPA-R removal underlies Aβ-induced synaptic depression and dendritic spine loss. Neuron 2006, 52(5):831-843.
96. Hu D., Serrano F., Oury T.D., Klann E. Aging-dependent alterations in synaptic plasticity and memory in mice that overexpress extracellular superoxide dismutase. J. Neurosci. 2006, 26(15):3933-3941.
97. Hu D., Cao P., Thiels E., Chu C.T., Wu G.Y., Oury T.D., Klann E. Hippocampal long-term potentiation, memory, and longevity in mice that overexpress mitochondrial superoxide dismutase. Neurobiol. Learn. Mem. 2007, 87(3):372-384.
98. Hua X., Leow A.D., Parikshak N., Lee S., Chiang M.C., Toga A.W., Jack C.R., Weiner M.W., Thompson P.M. Tensor-based morphometry as a neuroimaging biomarker for Alzheimer's disease: an MRI study of 676 AD, MCI, and normal subjects. Neuroimage 2008, 43(3):458-469.
99. Huddleston A.T., Tang W., Takeshima H., Hamilton S.L., Klann E. Superoxide-induced potentiation in the hippocampus requires activation of ryanodine receptor type 3 and ERK. J. Neurophysiol. 2008, 99(3):1565-1571.
100. Hung L.W., Ciccotosto G.D., Giannakis E., Tew D.J., Perez K., Masters C.L., Cappai R., Wade J.D., Barnham K.J. Amyloid-β peptide (Aβ) neurotoxicity is modulated by the rate of peptide aggregation: Aβ dimers and trimers correlate with neurotoxicity. J. Neurosci. 2008, 28(46):11950-11958.
101. Hussain I. APP transgenic mouse models and their use in drug discovery to evaluate amyloid-β lowering therapeutics. CNS Neurol. Disord. Drug Targets 2010, 9(4):395-402. (Review).
102. Hutton M., Lendon C.L., Rizzu P., Baker M., Froelich S., Houlden H., Pickering-Brown S., Chakraverty S., Isaacs A., Grover A., Hackett J., Adamson J., et al. Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17. Nature 1998, 393(6686):702-705.
103. Ittner L.M., Ke Y.D., Götz J. Phosphorylated Tau interacts with c-Jun N-terminal kinase-interacting protein 1 (JIP1) in Alzheimer disease. J. Biol. Chem. 2009, 284(31):20909-20916.
104. Ittner L.M., Ke Y.D., Delerue F., Bi M., Gladbach A., van Eersel J., Wölfing H., Chieng B.C., Christie M.J., Napier I.A., Eckert A., Staufenbiel M., et al. Dendritic function of tau mediates amyloid-β toxicity in Alzheimer's disease mouse models. Cell 2010, 142(3):387-397.
105. Jack C.R., Lowe V.J., Weigand S.D., Wiste H.J., Senjem M.L., Knopman D.S., Shiung M.M., Gunter J.L., Boeve B.F., Kemp B.J., Weiner M., Petersen R.C., et al. Serial PIB and MRI in normal, mild cognitive impairment and Alzheimer's disease: implications for sequence of pathological events in Alzheimer's disease. Brain 2009, 132(Pt 5):1355-1365.
106. Jacobsen J.S., Wu C.C., Redwine J.M., Comery T.A., Arias R., Bowlby M., Martone R., Morrison J.H., Pangalos M.N., Reinhart P.H., Bloom F.E. Early-onset behavioural and synaptic deficits in a mouse model of Alzheimer's disease. Proc. Natl. Acad. Sci. USA 2006, 103(13):5161-5166.
107. Jiang Y., Mullaney K.A., Peterhoff C.M., Che S., Schmidt S.D., Boyer-Boiteau A., Ginsberg S.D., Cataldo A.M., Mathews P.M., Nixon R.A. Alzheimer's-related endosome dysfunction in Down syndrome is Aβ-independent but requires APP and is reversed by BACE-1 inhibition. Proc. Natl. Acad. Sci. USA 2010, 107(4):1630-1635.
108. Kamenetz F., Tomita T., Hsieh H., Seabrook G., Borchelt D., Iwatsubo T., Sisodia S., Malinow R. APP processing and synaptic function. Neuron 2003, 37(6):925-937.
109. Khandogin J., Brooks C.L.I.I.I. Linking folding with aggregation in Alzheimer's β-amyloid peptides. Proc. Natl. Acad. Sci. USA 2007, 104(43):16880-16885.
110. Klann E., Roberson E.D., Knapp L.T., Sweatt J.D. A role for superoxide in protein kinase C activation and induction of long-term potentiation. J. Biol. Chem. 1998, 273(8):4516-4522.
111. Klein W.L., Krafft G.A., Finch C.E. Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum?. Trends Neurosci. 2001, 24(4):219-224. (Review).
112. Knapp L.T., Klann E. Potentiation of hippocampal synaptic transmission by superoxide requires the oxidative activation of protein kinase C. J. Neurosci. 2002, 22(3):674-683.
113. Koo E.H., Sisodia S.S., Archer D.R., Martin L.J., Weidemann A., Beyreuther K., Fischer P., Masters C.L., Price D.L. Precursor of amyloid protein in Alzheimer disease undergoes fast axonal transport. Proc. Natl. Acad. Sci. USA 1990, 87(4):1561-1565.
114. Kuo Y.M., Emmerling M.R., Vigo-Pelfrey C., Kasunic T.C., Kirkpatrick J.B., Murdoch G.H., Ball M.J., Roher A.E. Water-soluble Aβ (N-40, N-42) oligomers in normal and Alzheimer disease brains. J. Biol. Chem. 1996, 271(8):4077-4081.
115. Lacor P.N., Buniel M.C., Furlow P.W., Clemente A.S., Velasco P.T., Wood M., Viola K.L., Klein W.L. Aβ oligomer-induced aberrations in synaptic composition, shape, and density provide a molecular basis for loss of connectivity in Alzheimer's disease. J. Neurosci. 2007, 27(4):796-807.
116. LaFerla F.M., Green K.N., Oddo S. Intracellular amyloid-β in Alzheimer's disease. Nature Rev. Neurosci. 2007, 8(7):499-509. (Review).
117. 1-42 are potent central nervous system neurotoxins. Proc. Natl. Acad. Sci. USA 1998, 95(11):6448-6453.
118. Lambert J.C., et al. Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease. Nat. Genet. 2009, 41(10):1094-1099.
119. Lanz T.A., Carter D.B., Merchant K.M. Neurobiol. Dis. 2003, 13(3):246-253.
120. Lau L.F., Seymour P.A., Sanner M.A., Schachter J.B. Cdk5 as a drug target for the treatment of Alzheimer's disease. J. Mol. Neurosci. 2002, 19(3):267-273. (Review).
121. Lauren J., Gimbel D.A., Nygaard H.B., Gilbert J.W., Strittmatter S.M. Cellular prion protein mediates impairment of synaptic plasticity by amyloid-β oligomers. Nature 2009, 457(7233):1128-1132.
122. Lee V.M., Trojanowski J.Q. Progress from Alzheimer's tangles to pathological tau points towards more effective therapies now. J. Alzheimers Dis. 2006, 9(Suppl. 3):257-262. (Review).
123. Lee J.H., Yu W.H., Kumar A., Lee S., Mohan P.S., Peterhoff C.M., Wolfe D.M., Martinez-Vicente M., Massey A.C., Sovak G., Uchiyama Y., Westaway D., et al. Lysosomal proteolysis and autophagy require presenilin 1 and are disrupted by Alzheimer-related PS1 mutations. Cell 2010, 141(7):1146-1158.
124. Levy E., Carman M.D., Fernandez-Madrid I.J., Power M.D., Lieberburg I., van Duinen S.G., Bots G.T., Luyendijk W., Frangione B. Mutation of the Alzheimer's disease amyloid gene in hereditary cerebral hemorrhage, Dutch type. Science 1990, 248(4959):1124-1126.
125. Lewis J., McGowan E., Rockwood J., Melrose H., Nacharaju P., Van Slegtenhorst M., Gwinn-Hardy K., Paul Murphy M., Baker M., Yu X., Duff K., Hardy J., et al. Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein. Nat. Genet. 2000, 25(4):402-405.
126. Lewis J., Dickson D.W., Lin W.L., Chisholm L., Corral A., Jones G., Yen S.H., Sahara N., Skipper L., Yager D., Eckman C., Hardy J., et al. Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science 2001, 293(5534):1487-1491.
127. Li L., Chin L.-S., Shupliakov O., Brodin L., Sihra T.S., Hvalby Ø., Jensen V., Zheng D., McNamara J.O., Greengard P., Andersen P. Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice. Proc. Natl. Acad. Sci. USA 1995, 92(20):9235-9239.
128. Li F., Calingasan N.Y., Yu F., Mauck W.M., Toidze M., Almeida C.G., Takahashi R.H., Carlson G.A., Flint Beal M., Lin M.T., Gouras G.K. Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice. J. Neurochem. 2004, 89(5):1308-1312.
129. Li Y., Rinne J.O., Mosconi L., Pirraglia E., Rusinek H., DeSanti S., Kemppainen N., Någren K., Kim B.C., Tsui W., de Leon M.J. Regional analysis of FDG and PIB-PET images in normal aging, mild cognitive impairment, and Alzheimer's disease. Eur. J. Nucl. Med. Mol. Imaging 2008, 35(12):2169-2181.
130. Li S., Hong S., Shepardson N.E., Walsh D.M., Shankar G.M., Selkoe D. Soluble oligomers of amyloid β protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake. Neuron 2009, 62(6):788-801.
131. Li S., Jin M., Koeglsperger T., Shepardson N.E., Shankar G.M., Selkoe D.J. Soluble Aβ oligomers inhibit long-term potentiation through a mechanism involving excessive activation of extrasynaptic NR2B-containing NMDA receptors. J. Neurosci. 2011, 31(18):6627-6638.
132. Lin M.T., Beal M.F. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 2006, 443(7113):787-795. (Review).
133. Lin M.T., Simon D.K., Ahn C.H., Kim L.M., Beal M.F. High aggregate burden of somatic mtDNA point mutations in aging and Alzheimer's disease brain. Hum. Mol. Genet. 2002, 11(2):133-145.
134. Liou Y.-C., Sun A., Ryo A., Zhou X.-Z., Yu Z.-X., Huang H.K., Uchida T., Bronson R., Bing G., Li X., Hunter T., Lu K.P. Role of the prolyl isomerase Pin1 in protecting against age-dependent neurodegeneration. Nature 2003, 424(6948):556-561.
135. Litersky J.M., Johnson G.V.W. Phosphorylation by cAMP-dependent protein kinase inhibits the degradation of tau by calpain. J. Biol. Chem. 1992, 267(3):1563-1568.
136. Litterst C., Georgakopoulos A., Shioi J., Ghersi E., Wisniewski T., Wang R., Ludwig A., Robakis N.K. Ligand binding and calcium influx induce distinct ectodomain/γ-secretase-processing pathways of EphB2 receptor. J. Biol. Chem. 2007, 282(22):16155-16163.
137. Lovell M.A., Xiong S., Xie C., Davies P., Markesbery W.R. Induction of hyperphosphorylated tau in primary rat cortical neuron cultures mediated by oxidative stress and glycogen synthase kinase-3. J. Alzheimers Dis. 2004, 6(6):659-671.
138. Lu T., Pan Y., Kao S.Y., Li C., Kohane I., Chan J., Yankner B.A. Gene regulation and DNA damage in the ageing human brain. Nature 2004, 429(6994):883-891.
139. Lue L.F., Kuo Y.M., Roher A.E., Brachova L., Shen Y., Sue L., Beach T., Kurth J.H., Rydel R.E., Rogers J. Soluble amyloid β peptide concentration as a predictor of synaptic change in Alzheimer's disease. Am. J. Pathol. 1999, 155(3):853-862.
140. Lustbader J.W., Cirilli M., Lin C., Xu H.W., Takuma K., Wang N., Caspersen C., Chen X., Pollak S., Chaney M., Trinchese F., Liu S., et al. ABAD directly links Aβ to mitochondrial toxicity in Alzheimer's disease. Science 2004, 304(5669):448-452.
141. Ma T., Hoeffer C.A., Wong H., Massaad C.A., Zhou P., Iadecola C., Murphy M.P., Pautler R.G., Klann E. Amyloid β-induced impairments in hippocampal synaptic plasticity are rescued by decreasing mitochondrial superoxide. J. Neurosci. 2011, 31(15):5589-5595.
142. Manczak M., Anekonda T.S., Henson E., Park B.S., Quinn J., Reddy P.H. Mitochondria are a direct site of Aβ accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression. Hum. Mol. Genet. 2006, 15(9):1437-1449.
143. Mandelkow E., von Bergen M., Biernat J., Mandelkow E.M. Structural principles of tau and the paired helical filaments of Alzheimer's disease. Brain Pathol. 2007, 17(1):83-90. (Review).
144. Marambaud P., Robakis N.K. Genetic and molecular aspects of Alzheimer's disease shed light on new mechanisms of transcriptional regulation. Genes Brain Behav. 2005, 4(3):134-146. (Review).
145. Marambaud P., Wen P.H., Dutt A., Shioi J., Takashima A., Siman R., Robakis N.K. A CBP binding transcriptional repressor produced by the PS1/ε-cleavage of N-cadherin is inhibited by PS1 FAD mutations. Cell 2003, 114(5):635-645.
146. Marrosu M.G., Floris G., Costa G., Schirru L., Spinicci G., Cherchi M.V., Mura M., Mascia M.G., Cocco E. Dementia, pyramidal system involvement, and leukoencephalopathy with a presenilin 1 mutation. Neurology 2006, 66(1):108-111.
147. Massaad C.A., Washington T.M., Pautler R.G., Klann E. Overexpression of SOD-2 reduces hippocampal superoxide and prevents memory deficits in a mouse model of Alzheimer's disease. Proc. Natl. Acad. Sci. USA 2009, 106(32):13576-13581.
148. Matrone C., Ciotti M.T., Mercanti D., Marolda R., Calissano P. NGF and BDNF signaling control amyloidogenic route and Abeta production in hippocampal neurons. Proc. Natl. Acad. Sci. USA 2008, 105(35):13139-13144.
149. Mc Donald J.M., Savva G.M., Brayne C., Welzel A.T., Forster G., Shankar G.M., Selkoe D.J., Ince P.G., Walsh D.M. The presence of sodium dodecyl sulphate-stable Aβ dimmers is strongly associated with Alzheimer-type dementia. Brain 2010, 133(Pt 5):1328-1341.
150. McGeer P.L., McGeer E.G. NSAIDs and Alzheimer disease: epidemiological, animal model and clinical studies. Neurobiol. Aging 2007, 28(5):639-647. (Review).
151. McLean C.A., Cherny R.A., Fraser F.W., Fuller S.J., Smith M.J., Beyreuther K., Bush A.I., Masters C.L. Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease. Ann. Neurol. 1999, 46(6):860-866.
152. Melloni R.H., Apostolides P.J., Hamos J.E., DeGennaro L.J. Dynamics of synapsin I gene expression during the establishment and restoration of functional synapses in the rat hippocampus. Neuroscience 1994, 58(4):683-703.
153. Moechars D., Dewachter I., Lorent K., Reverse D., Baekelandt V., Naidu A., Tesseur I., Spittaels K., Van den Haute C.V., Checler F., Godaux E., Cordell B., et al. Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain. J. Biol. Chem. 1999, 274(10):6483-6492.
154. Molnar Z., Soos K., Lengyel I., Penke B., Szegedi V., Budai D. Enhancement of NMDA responses by β-amyloid peptides in the hippocampus in vivo. Neuroreport 2004, 15(10):1649-1652.
155. Morfini G., Szebenyi G., Elluru R., Ratner N., Brady S.T. Glycogen synthase kinase 3 phosphorylates kinesin light chains and negatively regulates kinesin-based motility. EMBO J. 2002, 21(3):281-293.
156. Morfini G.A., Burns M., Binder L.I., Kanaan N.M., LaPointe N., Bosco D.A., Brown R.H., Brown H., Tiwari A., Hayward L., Edgar J., Nave K.A., et al. Axonal transport defects in neurodegenerative diseases. J. Neurosci. 2009, 29(41):12776-12786. (Review).
157. 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation. J. Neurosci. 2000, 20(11):4050-4058.
158. Muresan V., Muresan Z. Is abnormal axonal transport a cause, a contributing factor or a consequence of the neuronal pathology in Alzheimer's disease?. Future Neurol. 2009, 4(6):761-773.
159. Murphy M.P. How mitochondria produce reactive oxygen species. Biochem. J. 2009, 417(1):1-13. (Review).
160. Newell K.L., Hyman B.T., Growdon J.H., Hedley-Whyte E.T. Application of the National Institute on Aging (NIA)-Reagan Institute criteria for the neuropathological diagnosis of Alzheimer disease. J. Neuropathol. Exp. Neurol. 1999, 58(11):1147-1155.
161. Nikolaev A., McLaughlin T., O'Leary D.D., Tessier-Lavigne M. APP binds DR6 to trigger axon pruning and neuron death via distinct caspases. Nature 2009, 457(7232):981-989.
162. Nixon R.A., Yang D.S., Lee J.H. Neurodegenerative lysosomal disorders: a continuum from development to late age. Autophagy 2008, 4(5):590-599. (Review).
163. Nunomura A., Perry G., Aliev G., Hirai K., Takeda A., Balraj E.K., Jones P.K., Ghanbari H., Wataya T., Shimohama S., Chiba S., Atwood C.S., et al. Oxidative damage is the earliest event in Alzheimer disease. J. Neuropathol. Exp. Neurol. 2001, 60(8):759-767.
164. O'Nuallain B., Freir D.B., Nicoll A.J., Risse E., Ferguson N., Herron C.E., Collinge J., Walsh D.M. Amyloid β-protein dimers rapidly form stable synaptotoxic protofibrils. J. Neurosci. 2010, 30(43):14411-14419.
165. Oakley H., Cole S.L., Logan S., Maus E., Shao P., Craft J., Guillozet-Bongaarts A., Ohno M., Disterhoft J., Van Eldik L., Berry R., Vassar R. Intraneuronal β-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. J. Neurosci. 2006, 26(4):10129-10140.
166. Oddo S., Caccamo A., Kitazawa M., Tseng B.P., LaFerla F.M. Amyloid deposition precedes tangle formation in a triple transgenic model of Alzheimer's disease. Neurobiol. Aging 2003, 24(8):1063-1070.
167. Oddo S., Caccamo A., Shepherd J.D., Murphy M.P., Golde T.E., Kayed R., Metherate R., Mattson M.P., Akbari Y., LaFerla F.M. Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Aβ and synaptic dysfunction. Neuron 2003, 39(3):409-421.
168. Ohyagi Y., Yamada T., Nishioka K., Clarke N.J., Tomlinson A.J., Naylor S., Nakabeppu Y., Kira J., Younkin S.G. Selective increase in cellular Aβ42 is related to apoptosis but not necrosis. Neuroreport 2000, 11(1):167-171.
169. Pak K., Chan S.L., Mattson M.P. Presenilin-1 mutation sensitizes oligodendrocytes to glutamate and amyloid toxicities, and exacerbates white matter damage and memory impairment in mice. Neuromolecular Med. 2003, 3(1):53-64.
170. Park H.-J., Seong Y.-M., Choi J.-Y., Kang S., Rhim H. Alzheimer's disease-associated amyloid β interacts with the human serine protease HtrA2/Omi. Neurosci. Lett. 2004, 357(1):63-67.
171. Parker W.D., Filley C.M., Parks J.K. Cytochrome oxidase deficiency in Alzheimer's disease. Neurology 1990, 40(8):1302-1303.
172. Pastorino L., Sun A., Lu P.J., Zhou X.Z., Balastik M., Finn G., Wulf G., Lim J., Li S.H., Li X., Xia W., Nicholson L.K., et al. The prolyl isomerase Pin1 regulates amyloid precursor protein processing and amyloid-β production. Nature 2006, 440(7083):528-534.
173. Pimplikar S.W., Nixon R.A., Robakis N.K., Shen J., Tsai L.H. Amyloid-independent mechanisms in Alzheimer's disease pathogenesis. J. Neurosci. 2010, 30(45):14946-14954. (Review).
174. Powers E.T., Powers D.L. Mechanisms of protein fibril formation: nucleated polymerization with competing off-pathway aggregation. Biophys. J. 2008, 94(2):379-391.
175. Praprotnik D., Smith M.A., Richey P.L., Vinters H.V., Perry G. Filament heterogeneity within the dystrophic neurites of senile plaques suggests blockage of fast axonal transport in Alzheimer's disease. Acta Neuropathol. 1996, 91(3):226-235.
176. Praticò D. Oxidative stress hypothesis in Alzheimer's disease: a reappraisal. Trends Pharmacol. Sci. 2008, 29(12):609-615.
177. Praticò D., Uryu K., Leight S., Trojanoswki J.Q., Lee V.M. Increased lipid peroxidation precedes amyloid plaque formation in an animal model of Alzheimer amyloidosis. J. Neurosci. 2001, 21(12):4183-4187.
178. Qin S., Hu X.-Y., Xu H., Zhou J.-N. Regional alteration of synapsin I in the hippocampal formation of Alzheimer's disease patients. Acta Neuropathol. 2004, 107(3):209-215.
179. Querfurth H.W., LaFerla F.M. Alzheimer's disease. N. Engl. J. Med. 2010, 362(4):329-344.
180. Rametti A., Esclaire F., Yardin C., Terro F. Linking alterations in tau phosphorylation and cleavage during neuronal apoptosis. J. Biol. Chem. 2004, 279(52):54518-54528.
181. Ramsden M., Kotilinek L., Forster C., Paulson J., McGowan E., SantaCruz K., Guimaraes A., Yue M., Lewis J., Carlson G., Hutton M., Ashe K.H. Age-dependent neurofibrillary tangle formation, neuron loss, and memory impairment in a mouse model of human tauopathy (P301L). J. Neurosci. 2005, 25(46):10637-10647.
182. Rapoport M., Dawson H.N., Binder L.I., Vitek M.P., Ferreira A. Tau is essential to β-amyloid-induced neurotoxicity. Proc. Natl. Acad. Sci. USA 2002, 99(9):6364-6369.
183. Raymond C.R., Ireland D.R., Abraham W.C. NMDA receptor regulation by amyloid-β does not account for its inhibition of LTP in rat hippocampus. Brain Res. 2003, 968(2):263-272.
184. Reddy P.H., McWeeney S., Park B.S., Manczak M., Gutala R.V., Partovi D., Jung Y., Yau V., Searles R., Mori M., Quinn J. Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer's disease. Hum. Mol. Genet. 2004, 13(12):1225-1240.
185. Reed-Geaghan E.G., Savage J.C., Hise A.G., Landreth G.E. CD14 and toll-like receptors 2 and 4 are required for fibrillar Aβ-stimulated microglial activation. J. Neurosci. 2009, 29(38):11982-11992.
186. Reed-Geaghan E.G., Reed Q.W., Cramer P.E., Landreth G.E. Deletion of CD14 attenuates Alzheimer's disease pathology by influencing the brain's inflammatory milieu. J. Neurosci. 2010, 30(46):15369-15373.
187. Rensink A.A., de Waal R.M., Kremer B., Verbeek M.M. Pathogenesis of cerebral amyloid angiopathy. Brain Res. Brain Res. Rev. 2003, 43(2):207-223. (Review).
188. Reynolds C.H., Garwood C.J., Wray S., Price C., Kellie S., Perera T., Zvelebil M., Yang A., Sheppard P.W., Varndell I.M., Hanger D.P., Anderton B.H. Phosphorylation regulates tau interactions with Src homology 3 domains of phosphatidylinositol 3-kinase, phospholipase Cgamma1, Grb2, and Src family kinases. J. Biol. Chem. 2008, 283(26):18177-18186.
189. Rhein V., Song X., Wiesner A., Ittner L.M., Baysang G., Meier F., Ozmen L., Bluethmann H., Dröse S., Brandt U., Savaskan E., Czech C., et al. Amyloid-β and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer's disease mice. Proc. Natl. Acad. Sci. USA 2009, 106(47):20057-20062.
190. Ribé E.M., Pérez M., Puig B., Gich I., Lim F., Cuadrado M., Sesma T., Catena S., Sánchez B., Nieto M., Gómez-Ramos P., Morán M.A., et al. Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice. Neurobiol. Dis. 2005, 20(3):814-822.
191. Richards J.G., Higgins G.A., Ouagazzal A.M., Ozmen L., Kew J.N., Bohrmann B., Malherbe P., Brockhaus M., Loetscher H., Czech C., Huber G., Bluethmann H., et al. PS2APP transgenic mice, coexpressing hPS2mut and hAPPswe, show age-related cognitive deficits associated with discrete brain amyloid deposition and inflammation. J. Neurosci. 2003, 23(26):8989-9003.
192. Richardson J.C., Kendal C.E., Anderson R., Priest F., Gower E., Soden P., Gray R., Topps S., Howlett D.R., Lavender D., Clarke N.J., Barnes J.C., et al. Ultrastructural and behavioural changes precede amyloid deposition in a transgenic model of Alzheimer's disease. Neuroscience 2003, 122(1):213-228.
193. Ringman J.M., O'Neill J., Geschwind D., Medina L., Apostolova L.G., Rodriguez Y., Schaffer B., Varpetian A., Tseng B., Ortiz F., Fitten J., Cummings J.L., et al. Diffusion tensor imaging in preclinical and presymptomatic carriers of familial Alzheimer's disease mutations. Brain 2007, 130(Part 7):1767-1776.
194. 11 C-PiB PET assessment of change in fibrillar amyloid-β load in patients with Alzheimer's disease treated with bapineuzumab: a phase 2, double-blind, placebo-controlled, ascending-dose study. Lancet Neurol. 2010, 9(4):363-372.
195. Robakis N.K. An Alzheimer's disease hypothesis based on transcriptional dysregulation. Amyloid 2003, 10(2):80-85. (Review).
196. Robakis N.K. Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives. Neurobiol. Aging 2011, 32(3):372-379.
197. Roberson E.D., Scearce-Levie K., Palop J.J., Yan F., Cheng I.H., Wu T., Gerstein H., Yu G.-Q., Mucke L. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model. Science 2007, 316(5825):750-754.
198. Roher A.E., Chaney M.O., Kuo Y.M., Webster S.D., Stine W.B., Haverkamp L.J., Woods A.S., Cotter R.J., Tuohy J.M., Krafft G.A., Bonnell B.S., Emmerling M.R. Morphology and toxicity of Aβ-(1-42) dimer derived from neuritic and vascular amyloid deposits in Alzheimer's disease. J. Biol. Chem. 1996, 271(34):20631-20635.
199. Rosin C., Bates T.E., Skaper S.D. Excitatory amino acid induced oligodendrocyte cell death in vitro: receptor-dependent and -independent mechanisms. J. Neurochem. 2004, 90(5):1173-1185.
200. Roth A.D., Ramirez G., Alarcón R., Von Bernhardi R. Oligodendrocytes damage in Alzheimer's disease: beta amyloid toxicity and inflammation. Biol. Res. 2005, 38(4):381-387. (Review).
201. Ruan H., Tang X.D., Chen M.-L., Joiner M.L., Sun G., Brot N., Weissbach H., Heinemann S.H., Iverson L., Wu C.-F., Hoshi T. High-quality life extension by the enzyme peptide methionine sulfoxide reductase. Proc. Natl. Acad. Sci. USA 2002, 99(10):2748-2753.
202. Ruberti F., Capsoni S., Comparini A., Di Daniel E., Franzot J., Gonfloni S., Rossi G., Berardi N., Cattaneo A. Phenotypic knockout of nerve growth factor in adult transgenic mice reveals severe deficits in basal forebrain cholinergic neurons, cell death in the spleen, and skeletal muscle dystrophy. J. Neurosci. 2000, 20(7):2589-2601.
203. Salter M.W., Kalia L.V. Src kinases: a hub for NMDA receptor regulation. Nat. Rev. Neurosci. 2004, 5(4):317-328. (Review).
204. Saura C.A., Choi S.Y., Beglopoulos V., Malkani S., Zhang D., Shankaranarayana Rao B.S., Chattarji S., Kelleher R.J., Kandel E.R., Duff K., Kirkwood A., Shen J. Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration. Neuron 2004, 42(1):23-36.
205. Scheuner D., Eckman C., Jensen M., Song X., Citron M., Suzuki N., Bird T.D., Hardy J., Hutton M., Kukull W., Larson E., Levy-Lahad E., et al. Secreted amyloid β-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease. Nat. Med. 1996, 2(8):864-870.
206. Schneider A., Mandelkow E. Tau-based treatment strategies in neurodegenerative diseases. Neurotherapeutics 2008, 5(3):443-457. (Review).
207. Schriner S.E., Linford N.J., Martin G.M., Treuting P., Ogburn C.E., Emond M., Coskun P.E., Ladiges W., Wolf N., Van Remmen H., Wallace D.C., Rabinovitch P.S. Extension of murine life span by overexpression of catalase targeted to mitochondria. Science 2005, 308(5730):1909-1911.
208. Selkoe D.J. Cell biology of the amyloid β-protein precursor and the mechanism of Alzheimer's disease. Annu. Rev. Cell Biol. 1994, 10:373-403. (Review).
209. Selkoe D.J. Translating cell biology into therapeutic advances in Alzheimer's disease. Nature 1999, 399(Suppl. 6738):A23-A31. (Review).
210. Selkoe D.J. Alzheimer's disease is a synaptic failure. Science 2002, 298(5594):789-791. (Review).
211. Selkoe D.J. Folding proteins in fatal ways. Nature 2003, 42(6968):900-904. (Review).
212. Shankar G.M., Walsh D.M. Alzheimer's disease: synaptic dysfunction and Aβ. Mol. Neurodegener. 2009, 4:48. 10.1186/1750-1326-4-48.
213. Shankar G.M., Bloodgood B.L., Townsend M., Walsh D.M., Selkoe D.J., Sabatini B.L. Natural oligomers of the Alzheimer amyloid-β protein induce reversible synaptic loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway. J. Neurosci. 2007, 27(11):2866-2875.
214. Shankar G.M., Li S., Mehta T.H., Garcia-Munoz A., Shepardson N.E., Smith I., Brett F.M., Farrell M.A., Rowan M.J., Lemere C.A., Regan C.M., Walsh D.M., et al. Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory. Nat. Med. 2008, 14(8):837-842.
215. Shen J. Impaired neurotransmitter release in Alzheimer's and Parkinson's diseases. Neurodegener. Dis. 2010, 7(1-3):80-83.
216. Sherrington R., Rogaev E.I., Liang Y., Rogaeva E.A., Levesque G., Ikeda M., Chi H., Lin C., Li G., Holman K., Tsuda T., Mar L., et al. Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature 1995, 375(6534):754-760.
217. Shioi J., Georgakopoulos A., Mehta P., Kouchi Z., Litterst C.M., Baki L., Robakis N.K. FAD mutants unable to increase neurotoxic Aβ 42 suggest that mutation effects on neurodegeneration may be independent of effects on Aβ. J. Neurochem. 2007, 101(3):674-681.
218. Shipton O.A., Leitz J.R., Dworzak J., Acton C.E., Tunbridge E.M., Denk F., Dawson H.N., Vitek M.P., Wade-Martins R., Paulsen O., Vargas-Caballero M. Tau protein is required for amyloid β-induced impairment of hippocampal long-term potentiation. J. Neurosci. 2011, 31(5):1688-1692.
219. Sinha G. Peering inside Alzheimer's brains. Nat. Biotechnol. 2011, 29(5):384-387.
220. Sisodia S.S., St George-Hyslop P.H. γ-Secretase, notch, Aβ and Alzheimer's disease: where do the presenilins fit in?. Nat. Rev. Neurosci. 2002, 3(4):281-290. (Review).
221. Snyder E.M., Nong Y., Almeida C.G., Paul S., Moran T., Choi E.Y., Nairn A.C., Salter M.W., Lombroso P.J., Gouras G.K., Greengard P. Regulation of NMDA receptor trafficking by amyloid-β. Nat. Neurosci. 2005, 8(8):1051-1058.
222. Song S.K., Kim J.H., Lin S.J., Brendza R.P., Holtzman D.M. Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition. Neurobiol. Dis. 2004, 15(3):640-647.
223. Sotiropoulos I., Catania C., Pinto L.G., Silva R., Pollerberg G.E., Takashima A., Sousa N., Almeida O.F.X. Stress acts cumulatively to precipitate Alzheimer's disease-like tau pathology and cognitive deficits. J. Neurosci. 2011, 31(21):7840-7847.
224. Spires T.L., Meyer-Luehmann M., Stern E.A., McLean P.J., Skoch J., Nguyen P.T., Bacskai B.J., Hyman B.T. Dendritic spine abnormalities in amyloid precursor protein transgenic mice demonstrated by gene transfer and intravital multiphoton microscopy. J. Neurosci. 2005, 25(31):7278-7287.
225. Stokin G.B., Lillo C., Falzone T.L., Brusch R.G., Rockenstein E., Mount S.L., Raman R., Davies P., Masliah E., Williams D.S., Goldstein L.S. Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease. Science 2005, 307(5713):1282-1288.
226. Sturchler-Pierrat C., Abramowski D., Duke M., Wiederhold K.H., Mistl C., Rothacher S., Ledermann B., Bürki K., Frey P., Paganetti P.A., Waridel C., Calhoun M.E., Jucker M., Probst A., Staufenbiel M., Sommer B. Proc. Natl. Acad. Sci. USA 1997, 94(24):13287-13292.
227. Sultana R., Boyd-Kimball D., Poon H.F., Cai J., Pierce W.M., Klein J.B., Markesbery W.R., Zhou X.Z., Lu K.P., Butterfield D.A. Oxidative modification and down-regulation of Pin1 in Alzheimer's disease hippocampus: a redox proteomics analysis. Neurobiol. Aging 2006, 27(7):918-925.
228. Sun J., Folk D., Bradley T.J., Tower J. Induced overexpression of mitochondrial Mn-superoxide dismutase extends the life span of adult Drosophila melanogaster. Genetics 2002, 161(2):661-672.
229. Suzuki K., Terry R.D. Fine structural localization of acid phosphatase in senile plaques in Alzheimer's presenile dementia. Acta Neuropathol. 1967, 8(3):276-284.
230. Swerdlow R.H., Parks J.K., Cassarino D.S., Maguire D.J., Maguire R.S., Bennett J.P., Davis R.E., Parker W.D. Cybrids in Alzheimer's disease: a cellular model of the disease?. Neurology 1997, 49(7):918-925.
231. Taguchi H., Planque S., Nishiyama Y., Symersky J., Boivin S., Szabo P., Friedland R.P., Ramsland P.A., Edmundson A.B., Weksler M.E., Paul S. Autoantibody-catalyzed hydrolysis of amyloid β peptide. J. Biol. Chem. 2008, 283(8):4714-4722.
232. Takahashi R.H., Almeida C.G., Kearney P.F., Yu F., Lin M.T., Milner T.A., Gouras G.K. Oligomerization of Alzheimer's β-amyloid within processes and synapses of cultured neurons and brain. J. Neurosci. 2004, 24(14):3592-3599.
233. Tamagno E., Parola M., Bardini P., Piccini A., Borghi R., Guglielmotto M., Santoro G., Davit A., Danni O., Smith M.A., Perry G., Tabaton M. β-Site APP cleaving enzyme up-regulation induced by 4-hydroxynonenal is mediated by stress-activated protein kinases pathways. J. Neurochem. 2005, 92(3):628-636.
234. Tanzi R.E. The synaptic Aβ hypothesis of Alzheimer disease. Nat. Neurosci. 2005, 8(8):977-979.
235. Terry R.D., Masliah E., Salmon D.P., Butters N., DeTeresa R., Hill R., Hansen L.A., Katzman R. Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment. Ann. Neurol. 1991, 30(4):572-580.
236. Terwel D., Muyllaert D., Dewachter I., Borghgraef P., Croes S., Devijver H., Van Leuven F. Amyloid activates GSK-3beta to aggravate neuronal tauopathy in bigenic mice. Am. J. Pathol. 2008, 172(3):786-798.
237. Thal D.R., Holzer M., Rüb U., Waldmann G., Günzel S., Zedlick D., Schober R. Alzheimer-related tau-pathology in the perforant path target zone and in the hippocampal stratum oriens and radiatum correlates with onset and degree of dementia. Exp. Neurol. 2000, 163(1):98-110.
238. Thiels E., Urban N.N., Gonzalez-Burgos G.R., Kanterewicz B.I., Barrionuevo G., Chu C.T., Oury T.D., Klann E. Impairment of long-term potentiation and associative memory in mice that overexpress extracellular superoxide dismutase. J. Neurosci. 2000, 20(20):7631-7639.
239. Ting J.T., Kelley B.G., Lambert T.J., Cook D.G., Sullivan J.M. Amyloid precursor protein overexpression depresses excitatory transmission through both presynaptic and postsynaptic mechanisms. Proc. Natl. Acad. Sci. USA 2007, 104(1):353-358.
240. Tomic J.L., Pensalfini A., Head E., Glabe C.G. Soluble fibrillar oligomer levels are elevated in Alzheimer's disease brain and correlate with cognitive dysfunction. Neurobiol. Dis. 2009, 35(3):352-358.
241. Tomiyama T., Matsuyama S., Iso H., Umeda T., Takuma H., Ohnishi K., Ishibashi K., Teraoka R., Sakama N., Yamashita T., Nishitsuji K., Ito K., et al. A mouse model of amyloid β oligomers: their contribution to synaptic alteration, abnormal tau phosphorylation, glial activation, and neuronal loss in vivo. J. Neurosci. 2010, 30(14):4845-4856.
242. Van Dam D., D'Hooge R., Staufenbiel M., Van Ginneken C., Van Meir F., De Deyn P.P. Age-dependent cognitive decline in the APP23 model precedes amyloid deposition. Eur. J. Neurosci. 2003, 17(2):388-396.
243. Vasilevko V., Xu F., Previti M., Van Nostrand W.E., Cribbs D.H. Experimental investigation of antibody-mediated clearance mechanisms of amyloid-β in CNS of Tg-SwDI transgenic mice. J. Neurosci. 2007, 27(49):13376-13383.
244. Velliquette R.A., O'Connor T., Vassar R. Energy inhibition elevates β-secretase levels and activity and is potentially amyloidogenic in APP transgenic mice: possible early events in Alzheimer's disease pathogenesis. J. Neurosci. 2005, 25(47):10874-10883.
245. Vossel K.A., Zhang K., Brodbeck J., Daub A.C., Sharma P., Finkbeiner S., Cui B., Mucke L. Tau reduction prevents Abeta-induced defects in axonal transport. Tau reduction prevents Aβ-induced defects in axonal transport. Science 2010, 330(6001):198.
246. Walsh D.M., Selkoe D.J. Deciphering the molecular basis of memory failure in Alzheimer's disease. Neuron 2004, 44(1):181-193. (Review).
247. Walsh D.M., Tseng B.P., Rydel R.E., Podlisny M.B., Selkoe D.J. The oligomerization of amyloid β-protein begins intracellularly in cells derived from human brain. Biochemistry 2000, 39(35):10831-10839.
248. Wang J., Dickson D.W., Trojanowski J.Q., Lee V.M. The levels of soluble versus insoluble brain Abeta distinguish Alzheimer's disease from normal and pathological aging. Exp. Neurol. 1999, 158(2):328-337.
249. Wang A., Das P., Switzer R.C., Golde T.E., Jankowsky J.L. Robust amyloid clearance in a mouse model of Alzheimer's disease provides novel insights into the mechanism of amyloid-β immunotherapy. J. Neurosci. 2011, 31(11):4124-4136.
250. Wang Y.-J., Wang X., Lu J.-J., Li Q.-X., Gao C.-Y., Liu X.-H., Sun Y., Yang M., Lim Y., Evin G., Zhong J.-H., Masters C., et al. p75NTR regulates Aβ deposition by increasing Aβ production but inhibiting Aβ aggregation with its extracellular domain. J. Neurosci. 2011, 31(6):2292-2304.
251. Weggen S., Eriksen J.L., Das P., Sagi S.A., Wang R., Pietrzik C.U., Findlay K.A., Smith T.E., Murphy M.P., Bulter T., Kang D.E., Marquez-Sterling N., et al. A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity. Nature 2001, 414(6860):212-216.
252. Wei W., Nguyen L.N., Kessels H.W., Hagiwara H., Sisodia S., Malinow R. Amyloid beta from axons and dendrites reduces local spine number and plasticity. Nat. Neurosci. 2010, 13(2):190-196.
253. Westerman M.A., Cooper-Blacketer D., Mariash A., Kotilinek L., Kawarabayashi T., Younkin L.H., Carlson G.A., Younkin S.G., Ashe K.H. The relationship between Aβ and memory in the Tg2576 mouse model of Alzheimer's disease. J. Neurosci. 2002, 22(5):1858-1867.
254. Whitehouse P.J., Price D.L., Struble R.G., Clark A.W., Coyle J.T., Delon M.R. Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain. Science 1982, 215(4537):1237-1239.
255. Winblad B., Wimo A. Pharmacoeconomics in Alzheimer's disease. Neurodegener. Dis. 2007, 4:5.
256. Wirths O., Weis J., Szczygielski J., Multhaup G., Bayer T.A. Axonopathy in an APP/PS1 transgenic mouse model of Alzheimer's disease. Acta Neuropathol. 2006, 111(4):312-319.
257. Wong E., Cuervo A.M. Autophagy gone awry in neurodegenerative diseases. Nat. Neurosci. 2010, 13(7):805-811. (Review).
258. Wyss-Coray T. Inflammation in Alzheimer disease: driving force, bystander or beneficial response?. Nat. Med. 2006, 12(9):1005-1015. (Review).
259. Yamada M., Itoh Y., Shintaku M., Kawamura J., Jensson O., Thorsteinsson L., Suematsu N., Matsushita M., Otomo E. Immune reactions associated with cerebral amyloid angiopathy. Stroke 1996, 27(7):1155-1162.
260. Yang D.S., Kumar A., Stavrides P., Peterson J., Peterhoff C.M., Pawlik M., Levy E., Cataldo A.M., Nixon R.A. Neuronal apoptosis and autophagy cross talk in aging PS/APP mice, a model of Alzheimer's disease. Am. J. Pathol. 2008, 173(3):665-681.
261. Yao J., Du H., Yan S., Fang F., Wang C., Lue L.-F., Guo L., Chen D., Stern D.M., Gunn Moore F.J., Xi Chen J., Arancio O., et al. Inhibition of amyloid-β (Aβ) peptide-binding alcohol dehydrogenase-Aβ interaction reduces Aβ accumulation and improves mitochondrial function in a mouse model of Alzheimer's disease. J. Neurosci. 2011, 31(6):2313-2320.
262. Yu W.H., Cuervo A.M., Kumar A., Peterhoff C.M., Schmidt S.D., Lee J.H., Mohan P.S., Mercken M., Farmery M.R., Tjernberg L.O., Jiang Y., Duff K., et al. Macroautophagy-a novel β-amyloid peptide-generating pathway activated in Alzheimer's disease. J. Cell Biol. 2005, 171(1):87-98.
263. 2+ elevation, missorting of endogenous Tau into dendrites, Tau phosphorylation, and destruction of microtubules and spines. J. Neurosci. 2010, 30(36):11938-11950.
264. Zhao D., Watson J.B., Xie C.W. Amyloid β prevents activation of calcium/calmodulin-dependent protein kinase II and AMPA receptor phosphorylation during hippocampal long-term potentiation. J. Neurophysiol. 2004, 92(5):2853-2858.
265. Zhu B., Luo L., Moore G.R., Paty D.W., Cynader M.S. Dendritic and synaptic pathology in experimental autoimmune encephalomyelitis. Am. J. Pathol. 2003, 162(5):1639-1650.