Aggregation, impaired degradation and immunization targeting of amyloid-beta dimers in Alzheimers disease: A stochastic modelling approach

Molecular Neurodegeneration

Volumn 7, Issue 1, 2012, Pages

  Proctor, Carole J ^a   Pienaar, Ilse Sanet ^a   Elson, Joanna L ^a   Kirkwood, Thomas Bl ^a  

^a NEWCASTLE UNIVERSITY   (United Kingdom)

Author keywords

Alzheimers disease; Amyloid beta; Dimers; Downs syndrome; Immunotherapy; Intervention; Mathematical model; Protein aggregation; Stochastic simulation

Indexed keywords

AMYLOID BETA PROTEIN; AMYLOID BETA PROTEIN[1-42]; ANTIBODY; ASPARTIC PROTEINASE INHIBITOR; DIMER; MONOMER; SECRETASE INHIBITOR; UNCLASSIFIED DRUG;

ADULT; AGING; ALZHEIMER DISEASE; AMYLOID PLAQUE; ARTICLE; BRAIN; COMPUTER SIMULATION; CONTROLLED STUDY; DIMERIZATION; DRUG EFFICACY; DRUG TARGETING; HUMAN; HUMAN CELL; IMMUNE RESPONSE; IMMUNIZATION; IMMUNOTHERAPY; IN VITRO STUDY; IN VIVO STUDY; MEDIATOR; PROTEIN AGGREGATION; PROTEIN DEGRADATION; PROTEIN METABOLISM; PROTEIN TARGETING; STOCHASTIC MODEL; SYMPTOM;

ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; HUMANS; IMMUNIZATION; MODELS, CHEMICAL; PROTEIN MULTIMERIZATION; PROTEOLYSIS;

EID: 84863095042     PISSN: None     EISSN: 17501326     Source Type: Journal    
DOI: 10.1186/1750-1326-7-32     Document Type: Article

References (57)

1. Alzheimers disease is a synaptic failure. Selkoe DJ, Science 2002 298 5594 789 791 10.1126/science.1074069 12399581
2. Neuropathological stageing of Alzheimer-related changes. Braak H, Braak E, Acta Neuropathol 1991 82 4 239 259 10.1007/BF00308809 1759558
3. Atrophy of the hippocampus, parietal cortex, and insula in Alzheimer's disease: a volumetric magnetic resonance imaging study. Foundas AL, Leonard CM, Mahoney SM, Agee OF, Heilman KM, Neuropsychiatry, neuropsychology, and behavioral neurology 1997 10 2 81 89 9150507
4. Plaques and tangles and the pathogenesis of Alzheimer's disease. Armstrong RA, Folia neuropathologica/Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences 2006 44 1 1 11 16565925
5. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease. Arriagada PV, Growdon JH, Hedley-Whyte ET, Hyman BT, Neurology 1992 42 3 Pt 1 631 639 1549228
6. The role of beta amyloid in Alzheimers disease: still a cause of everything or the only one who got caught? Verdile G, Fuller S, Atwood CS, Laws SM, Gandy SE, Martins RN, Pharmacological Research 2004 50 4 397 409 10.1016/j.phrs.2003.12.028 15304237
7. Amyloid, the presenilins and Alzheimer's disease. Hardy J, Trends Neurosci 1997 20 4 154 159 10.1016/S0166-2236(96)01030-2 9106355
8. Amyloid beta protein deposition in normal aging has the same characteristics as that in Alzheimers disease. Predominance of A beta 42(43) and association of A beta 40 with cored plaques. Fukumoto H, Asami-Odaka A, Suzuki N, Shimada H, Ihara Y, Iwatsubo T, Am J Pathol 1996 148 1 259 265 8546214
9. Occurrence of neuropathological changes and dementia of Alzheimer's disease in Down's syndrome. Wisniewski KE, Wisniewski HM, Wen GY, Ann Neurol 1985 17 3 278 282 10.1002/ana.410170310 3158266
10. The genetic defect causing familial Alzheimer's disease maps on chromosome 21. St George-Hyslop PH, Tanzi RE, Polinsky RJ, Haines JL, Nee L, Watkins PC, Myers RH, Feldman RG, Pollen D, Drachman D, et al. Science 1987 235 4791 885 890 10.1126/science.2880399 2880399
11. Plasma beta amyloid and the risk of Alzheimer's disease in Down syndrome. Coppus AM, Schuur M, Vergeer J, Janssens AC, Oostra BA, Verbeek MM, van Duijn CM, Neurobiol Aging 2011 http://dx.doi.org/10.1016/j.neurobiolaging.2011.08.007
12. Amyloid beta-protein fibrillogenesis. Detection of a protofibrillar intermediate. Walsh DM, Lomakin A, Benedek GB, Condron MM, Teplow DB, The Journal of biological chemistry 1997 272 35 22364 22372 10.1074/jbc.272.35.22364 9268388
13. Kinetic theory of fibrillogenesis of amyloid beta-protein. Lomakin A, Teplow DB, Kirschner DA, Benedek GB, Proc Natl Acad Sci U S A 1997 94 15 7942 7947 10.1073/pnas.94.15.7942 9223292
14. The amyloid state of proteins in human diseases. Eisenberg D, Jucker M, Cell 2012 148 6 1188 1203 10.1016/j.cell.2012.02.022 22424229
15. Targeting small Abeta oligomers: the solution to an Alzheimer's disease conundrum? Klein WL, Krafft GA, Finch CE, Trends Neurosci 2001 24 4 219 224 10.1016/S0166-2236(00)01749-5 11250006
16. Amyloid-b protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory. Shankar GM, Li S, Mehta TH, Garcia-Munoz A, Shepardson NE, Smith I, Brett FM, Farrell MA, Rowan MJ, Lemere CA, et al. Nat Med 2008 14 8 837 842 10.1038/nm1782 18568035
17. Amyloid beta protein dimer-containing human CSF disrupts synaptic plasticity: prevention by systemic passive immunization. Klyubin I, Betts V, Welzel AT, Blennow K, Zetterberg H, Wallin A, Lemere CA, Cullen WK, Peng Y, Wisniewski T, et al. J Neurosci 2008 28 16 4231 4237 10.1523/JNEUROSCI.5161-07. 2008 18417702
18. The presence of sodium dodecyl sulphate-stable A dimers is strongly associated with Alzheimer-type dementia. Mc Donald JM, Savva GM, Brayne C, Welzel AT, Forster G, Shankar GM, Selkoe DJ, Ince PG, Walsh DM, Brain 2010 133 5 1328 1341 10.1093/brain/awq065 20403962
19. Amyloid beta-protein dimers rapidly form stable synaptotoxic protofibrils. O'Nuallain B, Freir DB, Nicoll AJ, Risse E, Ferguson N, Herron CE, Collinge J, Walsh DM, J Neurosci 2010 30 43 14411 14419 10.1523/JNEUROSCI.3537- 10.2010 20980598
20. A monoclonal antibody against synthetic Abeta dimer assemblies neutralizes brain-derived synaptic plasticity-disrupting Abeta. O'Nuallain B, Klyubin I, Mc Donald JM, Foster JS, Welzel A, Barry A, Dykoski RK, Cleary JP, Gebbink MF, Rowan MJ, et al. J Neurochem 2011 119 1 189 201 10.1111/j.1471-4159. 2011.07389.x 21781116
21. Clearance mechanisms of Alzheimer's amyloid-[beta] peptide: implications for therapeutic design and diagnostic tests. Bates KA, Verdile G, Li QX, Ames D, Hudson P, Masters CL, Martins RN, Mol Psychiatry 2008 14 5 469 486 18794889
22. Decreased clearance of CNS beta-amyloid in Alzheimer's disease. Mawuenyega KG, Sigurdson W, Ovod V, Munsell L, Kasten T, Morris JC, Yarasheski KE, Bateman RJ, Science 2010 330 6012 1774 10.1126/science.1197623 21148344
23. Age-dependent decline of neprilysin in Alzheimer's disease and normal brain: inverse correlation with A beta levels. Hellstrom-Lindahl E, Ravid R, Nordberg A, Neurobiol Aging 2008 29 2 210 221 10.1016/j.neurobiolaging.2006.10. 010 17098332
24. Neprylisin decreases uniformly in Alzheimer's disease and in normal aging. Russo R, Borghi R, Markesbery W, Tabaton M, Piccini A, FEBS Lett 2005 579 27 6027 6030 10.1016/j.febslet.2005.09.054 16226260
25. Oxidized neprilysin in aging and Alzheimers disease brains. Wang D-S, Iwata N, Hama E, Saido TC, Dickson DW, Biochemical and Biophysical Research Communications 2003 310 1 236 241 10.1016/j.bbrc.2003.09.003 14511676
26. Changes with age in the activities of beta-secretase and the Abeta-degrading enzymes neprilysin, insulin-degrading enzyme and angiotensin-converting enzyme. Miners JS, van Helmond Z, Kehoe PG, Love S, Brain pathology (Zurich, Switzerland) 2010 20 4 794 802 10.1111/j.1750-3639.2010. 00375.x
27. Neprilysin and insulin-degrading enzyme levels are increased in Alzheimer disease in relation to disease severity. Miners JS, Baig S, Tayler H, Kehoe PG, Love S, J Neuropathol Exp Neurol 2009 68 8 902 914 10.1097/NEN.0b013e3181afe475 19606063
28. Abeta-degrading enzymes: potential for treatment of Alzheimer disease. Miners JS, Barua N, Kehoe PG, Gill S, Love S, J Neuropathol Exp Neurol 2011 70 11 944 959 10.1097/NEN.0b013e3182345e46 22002425
29. GSK3 and p53-is there a link in Alzheimer's disease? Proctor C, Gray D, Molecular Neurodegeneration 2010 5 1 7 10.1186/1750-1326-5-7 20181016
30. A mathematical model of aging-related and cortisol induced hippocampal dysfunction. McAuley MT, Kenny RA, Kirkwood TB, Wilkinson DJ, Jones JJ, Miller VM, BMC neuroscience 2009 10 26 10.1186/1471-2202-10-26 19320982
31. Modelling the role of the Hsp70/Hsp90 system in the maintenance of protein homeostasis. Proctor CJ, Lorimer IA, PLoS ONE 2011 6 7 22038 10.1371/journal.pone.0022038 21779370
32. A systematic look at an old problem. Kirkwood TB, Nature 2008 451 7179 644 647 10.1038/451644a 18256658
33. Effect of protein-protein interactions on protein aggregation kinetics. Zhang J, Liu XY, The Journal of Chemical Physics 2003 119 20 10972 10976 10.1063/1.1622380
34. A specific amyloid-beta protein assembly in the brain impairs memory. Lesne S, Koh MT, Kotilinek L, Kayed R, Glabe CG, Yang A, Gallagher M, Ashe KH, Nature 2006 440 7082 352 357 10.1038/nature04533 16541076
35. Critical role of soluble amyloid-beta for early hippocampal hyperactivity in a mouse model of Alzheimer's disease. Busche MA, Chen X, Henning HA, Reichwald J, Staufenbiel M, Sakmann B, Konnerth A, Proc Natl Acad Sci U S A 2012 109 22 8740 8745 10.1073/pnas.1206171109 22592800
36. Monoclonal antibodies that target pathological assemblies of Abeta. Lambert MP, Velasco PT, Chang L, Viola KL, Fernandez S, Lacor PN, Khuon D, Gong Y, Bigio EH, Shaw P, et al. J Neurochem 2007 100 1 23 35 10.1111/j.1471-4159. 2006.04157.x 17116235
37. Alzheimer's disease abeta vaccine reduces central nervous system abeta levels in a non-human primate, the Caribbean vervet. Lemere CA, Beierschmitt A, Iglesias M, Spooner ET, Bloom JK, Leverone JF, Zheng JB, Seabrook TJ, Louard D, Li D, et al. Am J Pathol 2004 165 1 283 297 10.1016/S0002-9440(10)63296-8 15215183
38. Developing novel immunogens for a safe and effective Alzheimer's disease vaccine. Lemere CA, Progress in brain research 2009 175 83 93 19660650
39. Amyloid precursor protein selective gamma-secretase inhibitors for treatment of Alzheimer's disease. Basi G, Hemphill S, Brigham E, Liao A, Aubele D, Baker J, Barbour R, Bova M, Chen X-H, Dappen M, et al. Alzheimer's research & therapy 2010 2 6 36 10.1186/alzrt60 22933741
40. Neuropathology of older persons without cognitive impairment from two community-based studies. Bennett DA, Schneider JA, Arvanitakis Z, Kelly JF, Aggarwal NT, Shah RC, Wilson RS, Neurology 2006 66 12 1837 1844 10.1212/01.wnl.0000219668.47116.e6 16801647
41. Tangle and neuron numbers, but not amyloid load, predict cognitive status in Alzheimer's disease. Giannakopoulos P, Herrmann FR, Bussiere T, Bouras C, Kovari E, Perl DP, Morrison JH, Gold G, Hof PR, Neurology 2003 60 9 1495 1500 10.1212/01.WNL.0000063311.58879.01 12743238
42. The distribution of tangles, plaques and related immunohistochemical markers in healthy aging and Alzheimer's disease. Price JL, Davis PB, Morris JC, White DL, Neurobiol Aging 1991 12 4 295 312 10.1016/0197-4580(91)90006-6 1961359
43. Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies. Adalbert R, Nogradi A, Babetto E, Janeckova L, Walker SA, Kerschensteiner M, Misgeld T, Coleman MP, Brain 2009 132 2 402 416 19059977
44. Beneficial effect of human anti-amyloid-b active immunization on neurite morphology and tau pathology. Serrano-Pozo A, William CM, Ferrer I, Uro-Coste E, Delisle M-B, Maurage C-A, Hock C, Nitsch RM, Masliah E, Growdon JH, et al. Brain 2010 133 5 1312 1327 10.1093/brain/awq056 20360050
45. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. Corder EH, Saunders AM, Strittmatter WJ, Schmechel DE, Gaskell PC, Small GW, Roses AD, Haines JL, Pericak-Vance MA, Science 1993 261 5123 921 923 10.1126/science.8346443 8346443
46. Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy. Bu G, Nat Rev Neurosci 2009 10 5 333 344 10.1038/nrn2620 19339974
47. Mitochondria are a direct site of A accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression. Manczak M, Anekonda TS, Henson E, Park BS, Quinn J, Reddy PH, Human Molecular Genetics 2006 15 9 1437 1449 10.1093/hmg/ddl066 16551656
48. Neprilysin Protects against Cerebral Amyloid Angiopathy and A-Induced Degeneration of Cerebrovascular Smooth Muscle Cells. Miners JS, Kehoe P, Love S, Brain Pathology 2011 21 5 594 605 21382117
49. Aggregation and disaggregation of senile plaques in Alzheimer disease. Cruz L, Urbanc B, Buldyrev SV, Christie R, Gámez-Isla T, Havlin S, McNamara M, Stanley HE, Hyman BT, Proceedings of the National Academy of Sciences 1997 94 14 7612 7616 10.1073/pnas.94.14.7612
50. On the nucleation and growth of amyloid beta-protein fibrils: detection of nuclei and quantitation of rate constants. Lomakin A, Chung DS, Benedek GB, Kirschner DA, Teplow DB, Proc Natl Acad Sci U S A 1996 93 3 1125 1129 10.1073/pnas.93.3.1125 8577726
51. Surfactant properties of Alzheimer's A beta peptides and the mechanism of amyloid aggregation. Soreghan B, Kosmoski J, Glabe C, Journal of Biological Chemistry 1994 269 46 28551 28554 7961799
52. The systems biology markup language (SBML): a medium for representation and exchange of biochemical network models. Hucka M, Finney A, Sauro HM, Bolouri H, Doyle JC, Kitano H, Arkin AP, Bornstein BJ, Bray D, and the rest of the SBML Forum, Bioinformatics 2003 19 4 524 531 10.1093/bioinformatics/btg015 12611808
53. Wilkinson DJ, Stochastic modelling for systems biology Chapman and Hall/CRC Press, Boca Raton, Florida second 2011
54. Two novel point mutations of mitochondrial tRNA genes in histologically confirmed Parkinson disease. Grasbon-Frodl EM, Kösel S, Sprinzl M, von Eitzen U, Mehraein P, Graeber MB, Neurogenetics 1999 2 2 121 127 10.1007/s100480050063 10369889
55. Biomodels Database [ http://www.ebi.ac.uk/biomodels ]
56. The Systems Biology Markup Language [ www.sbml.org ]
57. Exact stochastic simulation of coupled chemical reactions. Gillespie DT, The Journal of Physical Chemistry 1977 31 2340 2361