The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Calcium Dysregulation and Membrane Disruption as a Ubiquitous Neurotoxic Mechanism of Soluble Amyloid Oligomers*♦
Open accessAbstract
Increasing evidence suggests that amyloid peptides associated with a variety of degenerative diseases induce neurotoxicity in their intermediate oligomeric state, rather than as monomers or fibrils. To test this hypothesis and investigate the possible involvement of Ca2+ signaling disruptions in amyloid-induced cytotoxicity, we made homogeneous preparations of disease-related amyloids (Abeta, prion, islet amyloid polypeptide, polyglutamine, and lysozyme) in various aggregation states and tested their actions on fluo-3-loaded SH-SY5Y cells. Application of oligomeric forms of all amyloids tested (0.6-6 microg ml-1) rapidly (approximately 5 s) elevated intracellular Ca2+, whereas equivalent amounts of monomers and fibrils did not. Ca2+ signals evoked by Abeta42 oligomers persisted after depletion of intracellular Ca2+ stores, and small signals remained in Ca2+-free medium, indicating contributions from both extracellular and intracellular Ca2+ sources. The increased membrane permeability to Ca2+ cannot be attributed to activation of endogenous Ca2+ channels, because responses were unaffected by the potent Ca2+-channel blocker cobalt (20 microm). Instead, observations that Abeta42 and other oligomers caused rapid cellular leakage of anionic fluorescent dyes point to a generalized increase in membrane permeability. The resulting unregulated flux of ions and molecules may provide a common mechanism for oligomer-mediated toxicity in many amyloidogenic diseases, with dysregulation of Ca2+ ions playing a crucial role because of their strong trans-membrane concentration gradient and involvement in cell dysfunction and death.
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Cites
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Cited by
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The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes
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The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease
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Metadata
- Authors
- Demuro, A., Mina, E., Kayed, R., Milton, S. C., Parker, I., & Glabe, C. G.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2005-04
- Volume
- 280
- Issue
- 17
- Pages
- 17294-17300
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2129412868
- Cited by
- 1,041
- References
- 11
- FWCI
- 34.30
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Demuro, A., Mina, E., Kayed, R., Milton, S. C., Parker, I., & Glabe, C. G. (2005). Calcium Dysregulation and Membrane Disruption as a Ubiquitous Neurotoxic Mechanism of Soluble Amyloid Oligomers*♦. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m500997200
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