Pathogenesis of alzheimer's disease

Handbook of Neurotoxicity

Volumn 3, Issue , 2014, Pages 2327-2337

  Castellani, Rudy J ^a   Perry, George ^b  

^a UNIVERSITY OF MARYLAND   (United States)

^b UNIVERSITY OF TEXAS AT SAN ANTONIO   (United States)

Author keywords

Alzheimer disease; Amyloid beta; A ; Tau

Indexed keywords

EID: 84941095821     PISSN: None     EISSN: None     Source Type: Book    
DOI: 10.1007/978-1-4614-5836-4_162     Document Type: Chapter

References (50)

1. Alzheimer, A. (1907). Uber eine eigenartige erkrankung der himrinde. Allgemeine Zeits Psychiat PsychischYGerichtlich Med, 64, 146-148.
2. Arnold, S. E., Hyman, B. T., Flory, J., Damasio, A. R., & Van Hoesen, G. W. (1991). The topographical and neuroanatomical distribution of neurofibrillary tangles and neuritic plaques in the cerebral cortex of patients with Alzheimer's disease. Cerebral Cortex, 1(1), 103-116.
3. Baki, L., Marambaud, P., Efthimiopoulos, S., Georgakopoulos, A., Wen, P., Cui, W., et al. (2001). Presenilin-1 binds cytoplasmic epithelial cadherin, inhibits cadherin/p120 association, and regulates stability and function of the cadherin/catenin adhesion complex. Proceedings of the National Academy of Sciences of the United States of America, 98(5), 2381-2386.
4. Benilova, I., Karan, E., & De Strooper, B. (2012). The toxic Abeta oligomer and Alzheimer's disease: An emperor in need of clothes. Nature Neuroscience, 15(3), 349-357.
5. Berg, L., McKeel, D. W., Jr., Miller, J. P., Storandt, M., Rubin, E. H., Morris, J. C., et al. (1998). Clinicopathologic studies in cognitively healthy aging and Alzheimer's disease: Relation of Histologic markers to dementia severity, age, sex, and apolipoprotein E genotype. Archives of Neurology, 55(3), 326-335.
6. Blessed, G., Tomlinson, B. E., & Roth, M. (1968). The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects. The British Journal of Psychiatry, 114(512), 797-811.
7. Braak, H., & Braak, E. (1991). Neuropathological stageing of Alzheimer-related changes. Acta Neuropathologica, 82(4), 239-259.
8. Cairns, N. J., Bigio, E. H., Mackenzie, I. R., Neumann, M., Lee, V. M., Hatanpaa, K. J., et al. (2007). Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: Consensus of the consortium for frontotemporal lobar degeneration. Acta Neuropathologica, 114(1), 5-22.
9. Castellani, R. J., & Smith, M. A. (2011). Compounding artefacts with uncertainty, and an amyloid cascade hypothesis that is 'too big to fail'. Journal of Pathology, 224(2), 147-152.
10. Castellani, R. J., Rolston, R. K., & Smith, M. A. (2010). Alzheimer disease. Disease-a Month, 56(9), 484-546.
11. Castellani, R. J., Lee, H. G., Zhu, X., Perry, G., & Smith, M. A. (2008a). Alzheimer disease pathology as a host response. Journal of Neuropathology and Experimental Neurology, 67(6), 523-531.
12. Castellani, R. J., Nunomura, A., Lee, H. G., Perry, G., & Smith, M. A. (2008b). Phosphorylated tau: Toxic, protective, or none of the above. Journal of Alzheimer's Disease, 14(4), 377-383.
13. Castellani, R. J., Lee, H. G., Siedlak, S. L., Nunomura, A., Hayashi, T., Nakamura, M., et al. (2009). Reexamining Alzheimer's disease: Evidence for a protective role for amyloid-beta protein precursor and amyloid-beta. Journal of Alzheimer's Disease, 18(2), 447-452.
14. Cho, H. H., Cahill, C. M., Vanderburg, C. R., Scherzer, C. R., Wang, B., Huang, X., et al. (2010). Selective translational control of the Alzheimer amyloid precursor protein transcript by iron regulatory protein-1. Journal of Biological Chemistry, 285(41), 31217-31232.
15. Citron, M., Westaway, D., Xia, W., Carlson, G., Diehl, T., Levesque, G., et al. (1997). Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both Transfected cells and transgenic mice. Nature Medicine, 3(1), 67-72.
16. De Strooper, B., Annaert, W., Cupers, P., Saftig, P., Craessaerts, K., Mumm, J. S., et al. (1999). A presenilin-1-dependent gamma-secretase-like protease mediates release of notch intracellular domain. Nature, 398(6727), 518-522.
17. Duff, K., Eckman, C., Zehr, C., Yu, X., Prada, C. M., Perez-tur, J., et al. (1996). Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1. Nature, 383(6602), 710-713.
18. Giannakopoulos, P., Herrmann, F. R., Bussiere, T., Bouras, C., Kovari, E., Perl, D. P., et al. (2003). Tangle and neuron numbers, but not amyloid load, predict cognitive status in Alzheimer's disease. Neurology, 60(9), 1495-1500.
19. Glenner, G. G., & Wong, C. W. (1984). Alzheimer's disease and down's syndrome: Sharing of a unique cerebrovascular amyloid fibril protein. Biochemical and Biophysical Research Communications, 122(3), 1131-1135.
20. Grundke-Iqbal, I., Iqbal, K., Tung, Y. C., Quinlan, M., Wisniewski, H. M., & Binder, L. I. (1986). Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology. Proceedings of the National Academy of Sciences of the United States of America, 83(13), 4913-4917.
21. Hardy, J. A., & Higgins, G. A. (1992). Alzheimer's disease: The amyloid cascade hypothesis. Science, 256(5054), 184-185.
22. Hernandez, F., & Avila, J. (2007). Tauopathies. Cellular and Molecular Life Sciences, 64(17), 2219-2233.
23. Holmes, C., Boche, D., Wilkinson, D., Yadegarfar, G., Hopkins, V., Bayer, A., et al. (2008). Longterm effects of Abeta42 immunisation in Alzheimer's disease: Follow-up of a randomised, placebo-controlled phase I trial. Lancet, 372(9634), 216-223.
24. Kamal, A., Almenar-Queralt, A., LeBlanc, J. F., Roberts, E. A., & Goldstein, L. S. (2001). Kinesin-mediated axonal transport of a membrane compartment containing beta-secretase and presenilin-1 requires APP. Nature, 414(6864), 643-648.
25. Katayama, T., Imaizumi, K., Sato, N., Miyoshi, K., Kudo, T., Hitomi, J., Morihara, T., Yoneda, T., Gomi, F., Mori, Y., Nakano, Y., Takeda, J., Tsuda, T., Itoyama, Y., Murayama, O., Takashima, A., St George-Hyslop, P., Takeda, M., Tohyama, M. (1999). Presenilin-1 mutations downregulate the signalling pathway of the unfolded-protein response. Nat Cell Biol. 1(8), 479-85.
26. Ling, Y., Morgan, K., & Kalsheker, N. (2003). Amyloid precursor protein (APP) and the biology of proteolytic processing: Relevance to Alzheimer's disease. The International Journal of Biochemistry & Cell Biology, 35(11), 1505-1535.
27. Maiorini, A. F., Gaunt, M. J., Jacobsen, T. M., McKay, A. E., Waldman, L. D., & Raffa, R. B. (2002). Potential novel targets for Alzheimer pharmacotherapy: I secretases. Journal of Clinical Pharmacy and Therapeutics, 27(3), 169-183.
28. Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDonald, B. L., & Beyreuther, K. (1985). Amyloid plaque core protein in Alzheimer disease and down syndrome. Proceedings of the National Academy of Sciences of the United States of America, 82(12), 4245-4249.
29. Moller, H. J., & Graeber, M. B. (1998). The case described by alois Alzheimer in 1911. Historical and conceptual perspectives based on the clinical record and neurohistological sections. European Archives of Psychiatry and Clinical Neuroscience, 248(3), 111-122.
30. Montine, T. J., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Dickson, D. W., et al. (2012). National institute on Aging-Alzheimer's association guidelines for the neuropathologic assessment of Alzheimer's disease: A practical approach. Acta Neuropathologica, 123(1), 1-11.
31. Nelson, P. T., Alafuzoff, I., Bigio, E. H., Bouras, C., Braak, H., Cairns, N. J., et al. (2012). Correlation of Alzheimer disease neuropathologic changes with cognitive status: A review of the literature. Journal of Neuropathology & Experimental Neurology, 71(5), 362-381.
32. Nelson, P. T., Braak, H., & Markesbery, W. R. (2009). Neuropathology and cognitive impairment in Alzheimer disease: A complex but coherent relationship. Journal of Neuropathology and Experimental Neurology, 68(1), 1-14.
33. Niwa, M., Sidrauski, C., Kaufman, R. J., & Walter, P. (1999). A role for presenilin-1 in nuclear accumulation of Ire1 fragments and induction of the mammalian unfolded protein response. Cell, 99(7), 691-702.
34. Nunomura, A., Perry, G., Aliev, G., Hirai, K., Takeda, A., Balraj, E. K., et al. (2001). Oxidative damage is the earliest event in Alzheimer disease. Journal ofNeuropathology and Experimental Neurology, 60(8), 759-767.
35. Nunomura, A., Castellani, R. J., Zhu, X., Moreira, P. I., Perry, G., & Smith, M. A. (2006). Involvement of oxidative stress in Alzheimer disease. Journal of Neuropathology and Experimental Neurology, 65(7), 631-641.
36. Pietrzik, C. U., Yoon, I. S., Jaeger, S., Busse, T., Weggen, S., & Koo, E. H. (2004). FE65 Constitutes the functional link between the low-density lipoprotein receptor-related protein and the amyloid precursor protein. Journal of Neuroscience, 24(17), 4259-4265.
37. Santacruz, K., Lewis, J., Spires, T., Paulson, J., Kotilinek, L., Ingelsson, M., et al. (2005). Tau suppression in a neurodegenerative mouse model improves memory function. Science, 309(5733), 476-481.
38. Scheuner, D., Eckman, C., Jensen, M., Song, X., Citron, M., Suzuki, N., et al. (1996). Secreted amyloid beta-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. Nature Medicine, 2(8), 864-870.
39. Selkoe, D. J. (2008). Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. Behavioural Brain Research, 192(1), 106-113.
40. Smine, A., Xu, X., Nishiyama, K., Katada, T., Gambetti, P., Yadav, S. P., et al. (1998). Regulation of brain G-protein go by Alzheimer's disease gene presenilin-1. Journal of Biological Chemistry, 273(26), 16281-16288.
41. Spires-Jones, T. L., Stoothoff, W. H., de Calignon, A., Jones, P. B., & Hyman, B. T. (2009). Tau pathophysiology in neurodegeneration: A tangled issue. Trends in Neurosciences, 32(3), 150-159.
42. Stokin, G. B., Lillo, C., Falzone, T. L., Brusch, R. G., Rockenstein, E., Mount, S. L., et al. (2005). Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease. Science, 307(5713), 1282-1288.
43. Tanzi, R. E. (2005). The synaptic abeta hypothesis of Alzheimer disease. Nature Neuroscience, 8(8), 977-979.
44. Terry, R. D., Gonatas, N. K., & Weiss, M. (1964). Ultrastructural studies in Alzheimer's presenile dementia. American Journal of Pathology, 44, 269-297.
45. Vetrivel, K. S., & Thinakaran, G. (2006). Amyloidogenic processing of beta-amyloid precursor protein in intracellular compartments. Neurology, 66(2 Suppl. 1), S69-S73.
46. Walsh, D. M., Klyubin, I., Fadeeva, J. V., Cullen, W. K., Anwyl, R., Wolfe, M. S., et al. (2002). Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo. Nature, 416(6880), 535-539.
47. Wilkins, R. H., & Brody, I. A. (1969). Alzheimer's disease. Archives of Neurology, 21(1), 109-110.
48. Wilquet, V., & De Strooper, B. (2004). Amyloid-beta precursor protein processing in neurodegeneration. Current Opinion in Neurobiology, 14(5), 582-588.
49. Yoshiyama, Y., Higuchi, M., Zhang, B., Huang, S. M., Iwata, N., Saido, T. C., et al. (2007). Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model. Neuron, 53(3), 337-351.
50. Yu, G., Nishimura, M., Arawaka, S., Levitan, D., Zhang, L., Tandon, A., et al. (2000). Nicastrin modulates presenilin-mediated notch/glp-1 signal transduction and beta APP processing. Nature, 407(6800), 48-54.