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Behavioral and Neuropathologic Changes Induced by Central Injection of Carboxyl‐Terminal Fragment of β‐Amyloid Precursor Protein in Mice
Abstract
Abstract: Expression of the carboxyl‐terminal fragment (CT) of the β‐amyloid precursor protein (APP) in transgenic animals has been linked with neurotoxicity. However, it remains to be clarified whether the neurotoxicity is caused by β‐amyloid proteins (Aβs) derived from CT or by CT itself. To study the in vivo neurotoxicity of CT, mice were given a single intracerebroventricular injection of a recombinant 105‐amino acid CT (CT105; 68.5–685 pmol, intracerebroventricularly), and changes in behavior and in brain histology were examined. Animals given CT105 (410 or 685 pmol, intracerebroventricularly) showed a dose‐dependent impairment in the passive avoidance performance, whereas boiled CT105 had no effect. CT105 (685 pmol, intracerebroventricularly) induced reactive gliosis in neocortex and hippocampus and neurodegeneration in neocortex. These results indicate that centrally administered CT105 induces behavioral impairment and neuropathologic changes, suggesting a direct toxic effect of CT105 per se.
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Many studies using genetic or pharmacological approaches to increase C99 levels in animal models consistently demonstrate pathogenic properties of C99 linked with AD phenotypes.
“many studies using genetic or pharmacological approaches to increase C99 levels in animal models consistently demonstrate the pathogenic properties of C99 linked with AD phenotypes”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Song et al., 1998
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Research works printed but not linked: 4
- Kammesheidt A., Boyce F. M., Spanoyannis A. F., Cummings B. J., Ortegon M., Cotman C., Vaught J. L., and Neve R. L. (1992) Deposition of beta/A4 immunoreactivity and neuronal pathol- ogy in transgenic mice expressing the carboxy-terminal frag- ment of the Alzheimer amyloid precursor in the brain. Proc. Nati. Acad. Sci. USA 89, 10857-10861.
- Neve R. L., Kammesheidt A., and Hohmann C. F. (1992) Brain transplants of cells expressing the carboxyl-terminal fragment of the Alzheimer amyloid protein precursor cause specific neu- ropathology in vivo. Proc. Nail. Acad. Sci. USA 89, 3448- 3452.
- Selkoe D. 1., Podlisny M. B., Joachim C. L., Vickers E. A., Lee G., Fritz L. C., and Oltersdorf T. (1988) Beta-amyloid precursor protein of Alzheimer disease occurs as 110-to 135-kilodalton membrane-associated proteins in neural and nonneural tissues. Proc. Nail. Acad. Sci. USA 85, 7341-7345.
- Tamaoka A., Kalaria R. N., Lieberburg I., and Selkoe D. J. (1992) Identification of a stable fragment of the Alzheimer amyloid precursor containing the beta-protein in brain microvessels. Proc. Natl. Acad. Sci. USA 89, 1345-1349.
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Ohno, M., Cole, S. L., Yasvoina, M., Zhao, J., Citron, M., Berry, R., Disterhoft, J. F., & Vassar, R. (2007) · Neurobiology of Disease · doi:10.1016/j.nbd.2006.12.008 · Cited by 290
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Metadata
- Authors
- Song, D. ‐., Won, M. ‐., Jung, J. ‐., Lee, J. ‐., Kang, T. ‐., Suh, H. ‐., Huh, S. ‐., Paek, S. ‐., Kim, Y. ‐., Kim, S. ‐., & Suh, Y. ‐.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 1998-08
- Volume
- 71
- Issue
- 2
- Pages
- 875-878
- ISSN
- 0022-3042
- 1471-4159
- Cited by
- 58
- References
- 0
- Language
- en
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