Abstract
As noted in the introductory chapters of this book, neuritic plaques composed of accumulated amyloid β (Aβ) peptide are a hallmark pathological feature of the Alzheimer’s disease (AD) brain. Compelling genetic data now implicate these plaques as key causative agents in AD onset, as all known mutations that lead to early onset familial AD (1-6) result in an increased production of the amyloidogenic Aβ1-42 isoform (7-11). Although it appears likely that the deposition of multimeric Aβ fibrils into plaques is a necessary step in AD onset, there is still uncertainty as to how Aβ and neuritic plaques might cause the neuropathology that leads to the dementia that is characteristic of this disease.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Chartier-Harlin, M.-C., Crawford, F., Houlden, H., Warren, A., Hughes, D., Fidani, L., et al. (1991) Early-onset Alzheimer’s disease caused by mutations at codon 717 of the β-amyloid precursor protein gene. Nature 353, 844–845.
Goate, A., Chartier-Harlin, M.-C., Mullan, M., Brown, J., Crawford, F., Fidani, L., et al. (1991) Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer’s disease. Nature 349, 704–706.
Mullan, M., Crawford, F., Axelman, K., Houlden, H., Lilius, L., Winblad, B., and Lannfelt, L. (1992) A pathogenic mutation for probable Alzheimer’s disease in the APP gene at the N-terminus of β-amyloid. Nat. Genet. 1, 345–347.
Murrell, J., Farlow, M., Ghetti, B., and Benson, M. D. (1991) A mutation in the amyloid precursor protein associated with hereditary Alzheimer’s disease. Science 254, 97–99.
Levy-Lahad, E., Wasco, W., Poorkaj, P., Romano, D. M., Oshima, J., Pettingell, W. H., et al. (1995) Candidate gene for the chromosome 1 familial Alzheimer’s disease locus. Science 269, 973–977.
Sherrington, R., Rogaev, E. I., Liang, Y., Rogaeva, E. A., Levesque, G., Ikeda, M., et al. (1995) Cloning of a gene bearing missense mutations in early-onset familial Alzheimer’s disease. Nature 375, 754–760.
Cai, X.-D., Golde, T. E., and Younkin, S. G. (1993) Release of excess amyloid β protein from a mutant amyloid β protein precursor. Science 259 514–516.
Citron, M., Oltersdorf, T., Haass, C., McConlogue, L., Hung, A. Y., Seubert, P., et al. (1992) Mutation of the β-amyloid precursor protein in familial Alzheimer’s disease increases β-protein production. Nature 360, 672–674.
Suzuki, N., Cheung, T. T., Cai, X.-D., Odaka, A., Otvos, L., Eckman, C., et al. (1994) An increased percentage of long amyloid β protein secreted by familial amyloid β protein precursor (βAPP717) mutants. Science 264, 1336–1340.
Duff, K., Eckman, C., Zehr, C., Yu, X., Prada, C.-M., Perez-tur, J., et al. (1996) Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1. Nature 383, 710–713.
Scheuner, D., Eckman, C., Jensen, M., Song, X., Citron, M., Suzuki, N., et al. (1996) 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 in familial Alzheimer’s disease. Nat. Med. 2, 864–870.
Haga, S., Adai, K., and Ishii, T. (1989) Demonstration of microglial cells in and around senile (neuritic) plaques in the Alzheimer brain: an immunohistochemical study using a novel monoclonal antibody. Acta Neuropathol. 77, 569–575.
McGeer, P. L., Itagaki, S., Tago, H., and McGeer, E. G. (1987) Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histo-compatibility glycoprotein HLA-DR. Neurosci. Lett. 9, 195–200.
Rogers, J., Luber-Narod, J., Styren, S. D., and Civin, W. H. (1988) Expression of immune system-associated antigens by cells of the human central nervous system: relationship to the pathology of Alzheimer’s disease. Neurobiol. Aging 9, 339–349.
Griffin, W. S. T., Stanley, L. C., Ling. C., White, l., Macleod, V., Perrot, L., et al. (1989) Brain interleukin-1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease. Proc. Natl. Acad. Set USA 86, 7611–7615.
Itagaki, S., McGeer, P. L., Akiyama, H., Zhu, S., and Selkoe, D. J. (1989) Relationship of microglia and astrocytes to amyloid deposits of Alzheimer’s disease. J. Neuroimmunol. 24, 173–182.
Das, S. and Potter, H. (1995) Expression of the Alzheimer amyloid-promoting factor antichymotrypsin is induced in human astrocytes by IL-1. Neuron 14, 447–456.
Lee, S. C., Dickson, D. W., and Brosnan, C. F. (1995) Interleukin-1, nitric oxide and reactive astrocytes. Brain Behav. Immun. 9, 345–354.
Cacabelos, R., Alvarez, X. A., Fernandez-Novoa, L., Franco, A., Mangues, R., Pellicer, A., and Nishimura, T. (1993) Brain interleukin-1β in Alzheimer’s disease and vascular dementia. Methods Find. Exp. Clin. Pharmacol. 16, 141–151.
Blum-Degen, D., Muller, T., Kuhn, W., Gerlach, M., Przuntek, H., and Riederer, P. (1995) Interleukin-1β and interleukin-6 are elevated in the cerebrospinal fluid of Alzheimer’s and de novo Parkinson’s disease patients. Neurosci. Lett. 202, 17–20.
McGeer, P. L., Schulzer, M., and McGeer, E. G. (1996) Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer’s disease: areview of 17 epidemiologic studies. Neurology 47, 425–432.
Stewart, W. F., Kawas, C., Corrada, S. M., and Metter, E. J. (1997) Risk of Alzheimer’s disease and duration of NSAID use. Neurology 48, 626–632.
Araujo, D. M. and Cotman, C. W. (1992) β-Amyloid stimulates glial cells in vitro to produce growth factors that accumulate in senile plaques in Alzheimer’s disease. Brain Res. 569, 141–145.
Meda, L., Cassatella, M. A., Szendrel, G. I., Otvos, L., Baron, P., Villalba, M., et al. (1995) Activation of microglial cells by β-amyloid protein and interferon-γ. Nature 374, 647–650.
Yan, S. D., Chen, X., Fu, J., Chen, M., Zhu, H., Roher, A., et al. (1996) RAGE and amyloid-β peptide neurotoxicity in Alzheimer’s disease. Nature 382,685–691.
Lorton, D., Kocsis, J., King, L., Madden, K., and Brunden, K. R. (1996) β-Amyloid induces increased release of interleukin-1β from lipopolysaccharide-activated human monocytes. J. Neuroimmunol. 67, 21–29.
LeVine, H. (1993) Thioflavine T interaction with synthetic Alzheimer’s disease β-amyloid peptides: detection of amyloid aggregation in solution. Protein Sci. 2, 404–410.
Gupta-Bansal, R. and Brunden, K. R. (1998) Congo red inhibits proteoglycan and serum amyloid P binding to amyloid β fibrils. J. Neurochem. 70, 292–298.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2000 Humana Press Inc., Totowa, NJ
About this protocol
Cite this protocol
Brunden, K.R., Kocsis-Angle, J., Embury, P., Yates, S.L. (2000). Aβ-Induced Proinflammatory Cytokine Release from Differentiated Human THP-1 Monocytes. In: Hooper, N.M. (eds) Alzheimer's Disease. Methods in Molecular Medicine™, vol 32. Humana Press. https://doi.org/10.1385/1-59259-195-7:101
Download citation
DOI: https://doi.org/10.1385/1-59259-195-7:101
Publisher Name: Humana Press
Print ISBN: 978-0-89603-737-3
Online ISBN: 978-1-59259-195-4
eBook Packages: Springer Protocols