The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
Amyloid Fibrils Activate Tyrosine Kinase-Dependent Signaling and Superoxide Production in Microglia
Open accessAbstract
Alzheimer’s disease (AD) is a devastating neurological disorder characterized by loss of cognitive skills and progressive dementia. The pathological hallmark of AD is the presence of numerous senile plaques throughout the hippocampus and cerebral cortex associated with degenerating axons, neurofibrillary tangles, and gliosis. The core of the senile plaque primarily is composed of the 39–43 amino acid β-amyloid peptide (Aβ), which forms fibrils of β-pleated sheets. Although considerable genetic evidence implicates Aβ in the pathogenesis of AD, a direct causal link remains to be established. Senile plaques are foci of local inflammatory processes, as evidenced by the presence of numerous activated microglia and acute phase proteins. Aβ has been shown to elicit inflammatory responses in microglia; however, the intracellular events mediating these effects are largely unknown. We report that exposure of microglia and THP1 monocytes to fibrillar Aβ led to time- and dose-dependent increases in protein tyrosine phosphorylation of a population of proteins similar to that elicited by classical immune stimuli such as immune complexes. The tyrosine kinases Lyn, Syk, and FAK were activated on exposure of microglia and THP1 monocytes to Aβ, resulting in the tyrosine kinase-dependent generation of superoxide radicals. The present data support a role for oxidative damage in the pathogenesis of AD, provide an important mechanistic link between Aβ and the generation of reactive oxygen intermediates, and identify molecular targets for therapeutic intervention in AD.
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Cites
Bradford, M. M. (1976) · Analytical Biochemistry · doi:10.1016/0003-2697(76)90527-3 · Cited by 255,302
Glenner, G. G., & Wong, C. W. (1984) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(84)80190-4 · Cited by 5,404
Amyloid plaque core protein in Alzheimer disease and Down syndrome.
Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDonald, B. L., & Beyreuther, K. (1985) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.82.12.4245 · Cited by 4,431
Reactive Oxygen Species and the Central Nervous System
Halliwell, B. (1992) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1992.tb10990.x · Cited by 2,947
Integrins and Signal Transduction Pathways: the Road Taken
Clark, E. A., & Brugge, J. S. (1995) · Science · doi:10.1126/science.7716514 · Cited by 2,937
The molecular pathology of Alzheimer's disease
Selkoe, D. J. (1991) · Neuron · doi:10.1016/0896-6273(91)90052-2 · Cited by 2,708
RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease
Yan, S. D., Chen, X., Fu, J., Chen, M., Zhu, H., Roher, A., Slattery, T., Zhao, L., Nagashima, M., Morser, J., et al. (1996) · Nature · doi:10.1038/382685a0 · Cited by 2,012
Reduced cell motility and enhanced focal adhesion contact formation in cells from FAK-deficient mice
llić, D., Furuta, Y., Kanazawa, S., Takeda, N., Sobue, K., Nakatsuji, N., Nomura, S., Fujimoto, J., Okada, M., Yamamoto, T., et al. (1995) · Nature · doi:10.1038/377539a0 · Cited by 1,830
Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease.
Griffin, W. S., Stanley, L. C., Ling, C., White, L., MacLeod, V, Perrot, L. J., White, C. L., & Araoz, C. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.19.7611 · Cited by 1,777
Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state
Pike, C., Burdick, D., Walencewicz, A., Glabe, C., & Cotman, C. (1993) · The Journal of Neuroscience · doi:10.1523/jneurosci.13-04-01676.1993 · Cited by 1,417
Cited by
Polazzi, E., Mengoni, I., Caprini, M., Peña-Altamira, E., Kurtys, E., & Monti, B. (2013) · Neurosignals · doi:10.1159/000337115 · Cited by 8,994
Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514
Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
Lambert, M. P., Barlow, A. K., Chromy, B. A., Edwards, C., Freed, R., Liosatos, M., Morgan, T. E., Rozovsky, I., Trommer, B., Viola, K. L., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.11.6448 · Cited by 3,506
Role of Pro-Inflammatory Cytokines Released from Microglia in Neurodegenerative Diseases
Smith, J. A., Das, A., Ray, S. K., & Banik, N. L. (2012) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2011.10.004 · Cited by 1,165
Oxidative stress and Alzheimer disease
Christen, Y. (2000) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/71.2.621s · Cited by 1,158
Metadata
- Authors
- McDonald, D. R., Brunden, K. R., & Landreth, G. E.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1997-04-01
- Volume
- 17
- Issue
- 7
- Pages
- 2284-2294
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2159027833
- Cited by
- 317
- References
- 61
- FWCI
- 8.42
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- McDonald, D. R., Brunden, K. R., & Landreth, G. E. (1997). Amyloid Fibrils Activate Tyrosine Kinase-Dependent Signaling and Superoxide Production in Microglia. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.17-07-02284.1997
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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