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 facilitate a positive feedback loop of increasing oxidative stress and elevated Aβ levels, leading to neuritic dystrophy and neuronal death.
“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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Deposition of amyloid fibrils promotes cell-surface accumulation of amyloid β precursor protein
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“In addition, Ah fibrils specifically induce neuronal dystrophy (Busciglio et al., 1993; Grace et al., 2002; Pigino et al., 2001; Pike et al., 1992) characterized by abnormal focal adhesion- related protein activation and aberrant focal adhesion-like (FA-like) structures formation (Grace and…”
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Development and Expression of Amyloid‐β Peptide 42 in Retinal Ganglion Cells in Rats
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“In vitro studies also showed that a high dose of Ab-42 induced neuronal degeneration and neurapophysis retraction (Pike et al., 1992; Dahlgren et al., 2002).”
BackgroundNEURON DEGENERATION INDUCED BY VERAPAMIL AND ATTENUATED BY EGb761
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Self-citation
- 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
- Health Sciences › Medicine › Physiology › 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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