The DOI matches its Crossref record; 216 of the 216 references it cites were found in a registry or an index.
Biochemistry of Amyloid -Protein and Amyloid Deposits in Alzheimer Disease
Open accessAbstract
Progressive cerebral deposition of the amyloid β-protein (Aβ) in brain regions serving memory and cognition is an invariant and defining feature of Alzheimer disease. A highly similar but less robust process accompanies brain aging in many nondemented humans, lower primates, and some other mammals. The discovery of Aβ as the subunit of the amyloid fibrils in meningocerebral blood vessels and parenchymal plaques has led to innumerable studies of its biochemistry and potential cytotoxic properties. Here we will review the discovery of Aβ, numerous aspects of its complex biochemistry, and current attempts to understand how a range of Aβ assemblies, including soluble oligomers and insoluble fibrils, may precipitate and promote neuronal and glial alterations that underlie the development of dementia. Although the role of Aβ as a key molecular factor in the etiology of Alzheimer disease remains controversial, clinical trials of amyloid-lowering agents, reviewed elsewhere in this book, are poised to resolve the question of its pathogenic primacy.
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1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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RetractedAmyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
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Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide
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Self-citationThe precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
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Self-citationAmyloid plaque core protein in Alzheimer disease and Down syndrome.
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Self-citationCorrelative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
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Self-citationDiffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
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Neuropathological alterations in Alzheimer disease
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Cited by
Alzheimer Disease: An Update on Pathobiology and Treatment Strategies
Long, J. M., & Holtzman, D. M. (2019) · Cell · doi:10.1016/j.cell.2019.09.001 · Cited by 3,204
The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease
Spires-Jones, T. L., & Hyman, B. T. (2014) · Neuron · doi:10.1016/j.neuron.2014.05.004 · Cited by 1,201
Microglia constitute a barrier that prevents neurotoxic protofibrillar Aβ42 hotspots around plaques
Condello, C., Yuan, P., Schain, A., & Grutzendler, J. (2015) · Nature Communications · doi:10.1038/ncomms7176 · Cited by 718
Amyloid β Protein and Alzheimer’s Disease: When Computer Simulations Complement Experimental Studies
Nasica-Labouze, J., Nguyen, P. H., Sterpone, F., Berthoumieu, O., Buchete, N.-V., Coté, S., De Simone, A., Doig, A. J., Faller, P., Garcia, A., et al. (2015) · Chemical Reviews · doi:10.1021/cr500638n · Cited by 584
The preclinical phase of the pathological process underlying sporadic Alzheimer’s disease
Braak, H., & Del Tredici, K. (2015) · Brain · doi:10.1093/brain/awv236 · Cited by 540
Metadata
- Authors
- Masters, C. L., & Selkoe, D. J.
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-02-21
- Volume
- 2
- Issue
- 6
- Pages
- a006262-a006262
- ISSN
- 2157-1422 (ISSN-L)
- OpenAlex
- W2132815274
- Cited by
- 542
- References
- 216
- Type
- posted content
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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