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β-Amyloid induces neuritic dystrophy in vitro: similarities with Alzheimer pathology
Abstract
beta-Amyloid protein, the major component of neuritic plaques found in Alzheimer's disease, has been implicated as a potential contributor to the disease's progressive neuropathology. We report that within a two day exposure to aggregates of synthetic beta-amyloid peptide, the neurites of cultured rat hippocampal neurons adopt a dystrophic appearance. Observed morphological changes in the neurites include beading, fragmentation, terminal swelling and tortuous growth patterns. The degenerative changes are similar to those observed in neurites associated with neuritic plaques, suggesting that beta-amyloid may induce the neuritic abnormalities of Alzheimer neuropathology.
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“Aβ plaques also play a role in facilitating a positive feedback loop of increasing oxidative stress and subsequently elevated Aβ levels, leading to neuritic dystrophy and culminating in neuronal death [16,17,18,19].”
From Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice (2019) · cites this paper as [19]
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Items 101–131 of 131
Tsering, W., Hery, G. P., Phillips, J. L., Lolo, K., Bathe, T., Villareal, J. A. B., Ruan, I. Y., & Prokop, S. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01688-6 · Cited by 15
“The first hypothesis is based on Aβ oligomer studies suggesting the exogenous application of Aβ oligomers in cell culture models resulted in beaded neurites with disruption in microtubules and axonal transport [2, 57, 61].”
BackgroundUemura, M., & Ishiguro, H. (2015) · Cryobiology · doi:10.1016/j.cryobiol.2015.01.006 · Cited by 14
Apoptosis and Alzheimer’s Disease
LeBlanc, A. C. (1997) · Humana Press eBooks · doi:10.1007/978-1-59259-471-9_5 · Cited by 13
Monnerie, H., Esquenazi, S., Shashidhara, S., & Roux, P. D. L. (2005) · Neurological Research · doi:10.1179/016164105x40020 · Cited by 10
Lain, E., Penke, B., Delacourte, A., Gündisch, D., Schröder, H., & Witter, B. (2005) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2005.03909.x · Cited by 10
“These observations are consistent with previous studies on hippocampal primary cultures treated with fibrillary Ab, which reported similar findings (Yankner et al., 1990; Pike et al., 1992; Lorenzo & Yankner, 1994).”
ResultApoptosis in Alzheimer’s Disease
Cotman, C. W., & Pike, C. J. (1998) · Advances in behavioral biology · doi:10.1007/978-1-4615-5337-3_8 · Cited by 9
Self-citationMansor, N. I., Ntimi, C. M., Abdul-Aziz, N. M., Ling, K., Adam, A., Rosli, R., Hassan, Z., & Nordin, N. (2020) · Bosnian Journal of Basic Medical Sciences · doi:10.17305/bjbms.2020.4639 · Cited by 9
“The accumulation of Aβ1-42 peptides in neurites resulted in the formation of neuritic plaque and ultimately neurite degeneration [67].”
BackgroundProtective effects of ω-conotoxin on Amyloid-β-induced damage in PC12 cells
Fang, M., Wang, J., Han, S., et al. (2011) · Toxicology Letters · doi:10.1016/j.toxlet.2011.07.022 · Cited by 8
Differential roles of Aβ processing in hypoxia-induced axonal damage
Christianson, M. G., & Lo, D. C. (2015) · Neurobiology of Disease · doi:10.1016/j.nbd.2015.02.027 · Cited by 7
“Aβ itself impairs axonal structure and function in a variety of experimental paradigms (Kasa et al., 2000; Pike et al., 1992; Stokin et al., 2005), and blockade of the enzymes necessary for Aβ production from APP (BACE1 and the γ-secretase complex (Hardy and Selkoe, 2002; Scheuner et al., 1996;…”
BackgroundChapter 6. Perspectives on Amyloid and Alzheimer's Disease: A Critical Review
Krafft, G. A. (1993) · Annual reports in medicinal chemistry · doi:10.1016/s0065-7743(08)60876-3 · Cited by 7
The β-Amyloid Model of Alzheimer’s Disease
Cotman, C. W., Cribbs, D. H., & Anderson, A. J. (1997) · Humana Press eBooks · doi:10.1007/978-1-59259-471-9_6 · Cited by 5
Self-citationFogle, J. E., Hudson, L. C., Thomson, A., Sherman, B. L., Gruen, M. E., Lascelles, B. D. X., Colby, B., Clary, G., Longo, F. M., & Meeker, R. B. (2021) · Journal of NeuroVirology · doi:10.1007/s13365-021-00956-2 · Cited by 5
Wen, F., Nie, D., Hu, K., Tang, G., Yao, S., & Tang, C. (2017) · BMC Medical Imaging · doi:10.1186/s12880-017-0200-1 · Cited by 4
Kása, P., Papp, H., Zombori, J., Mayer, P. E., & Checler, F. (2003) · Neurochemical Research · doi:10.1023/a:1022813104905 · Cited by 2
“Our suggestion is supported by the result of an in vitro experiment, in which the nonaggregated C-terminal domain of Ab (Ab29-42) induced the neuronal cell death of rat hippocampal neurons in primary cultures (3).”
BackgroundResultCellular Signaling Pathways in Neuronal Apoptosis
Cotman, C. W., Qian, H., & Anderson, A. J. (2000) · doi:10.1007/978-1-59259-019-3_7 · Cited by 3
Self-citationPlioplys, A. V. (1995) · Journal of the Neurological Sciences · doi:10.1016/0022-510x(95)00171-w · Cited by 2
“, 1991) and to induce neuritic dystrophy in cultured rat hippocampal neurons (Pike et al., 1992).”
BackgroundLichtenstein, K. A. (2008) · CRC Press eBooks · doi:10.3109/9781420065985-5 · Cited by 1
Signaling Mechanisms that Mediate Aβ Induced Neuronal Dysfunction
Cotman, C. W., & Busciglio, J. A. (2007) · Springer eBooks · doi:10.1007/978-0-387-35135-3_8
Self-citationCotman, C. W., & Cummings, B. J. (1999) · Elsevier eBooks · doi:10.1016/b978-012705070-6/50022-6
Self-citationCotman, C. W., Cribbs, D. H., & Su, J. H. (1997) · Birkhäuser Boston eBooks · doi:10.1007/978-1-4612-4116-4_16
Self-citationLain, E. (2004) · Kölner Universitäts PublikationsServer (Universität zu Köln)
Zhu, C., Xu, Y., Zhang, P., Wang, M., Liu, J., & Wu, K. (2010) · International Conference on Bioinformatics and Biomedical Technology (ICBBT) · doi:10.1109/icbbt.2010.5478934
Hölscher, C., Herron, C. E., Alkadhi, K. A., et al. (2015)
Busciglio, J. A., & Deshpande, A. M. (2008) · Oxford University Press eBooks · doi:10.1093/acprof:oso/9780195369007.003.0010
Silva, C. S. (2015) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) · doi:10.34626/8a45-jz73
Potier, B., Dutar, P., & Lamour, Y. A. (1994) · Springer eBooks · doi:10.1007/978-3-662-01135-5_6
Achim, C. L., & Everall, I. (2008) · CRC Press eBooks · doi:10.3109/9781420065985-3
Potential anti-amyloid beta oligomerization effects of PD166793 in Alzheimer's disease
Kim, D., Shim, K., Kim, J., Ko, G., Tan, M. A., Chang, K.-A., & An, S. S. A. (2025) · Experimental Neurology · doi:10.1016/j.expneurol.2025.115504
Tsering, W., Hery, G. P., Phillips, J. L., Lolo, K., Bathe, T., Villareal, J. A. B., Ruan, I. Y., & Prokop, S. (2024) · Figshare · doi:10.6084/m9.figshare.26648013
Metadata
- Authors
- Pike, C. J., Cummings, B. J., & Cotman, C. W.
- Affiliations
- University of California, Irvine (US)
- Venue
- Neuroreport
- Published
- 1992-09
- Volume
- 3
- Issue
- 9
- Pages
- 769-772
- ISSN
- 0959-4965 (ISSN-L)
- OpenAlex
- W2017132797
- Cited by
- 131
- References
- 0
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 5 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 1 · 2018: 1 · 2017: 3 · 2016: 1 · 2015: 5 · 2014: 2 · 2013: 2
- FWCI
- 4.76
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroreport (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1r35ag007918-01)
- National Institute on Aging (AG07918)
- National Institute of Mental Health (MH 14599, T32MH014599)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- amyloid-beta, neuritic dystrophy, neurite degeneration, neuritic plaques, Alzheimer's disease, hippocampal neurons, neurite morphology, neurotoxicity
- MeSH terms
- Alzheimer Disease, Animals, Microscopy, Electron, Nerve Degeneration, Amyloid beta-Peptides, Neurites, Rats, Sprague-Dawley, Culture Techniques, Rats
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