Breaking the Code of Amyloid-β Oligomers
Author
Source
International Journal of Cell Biology
Issue
Vol. 2013, Issue 2013 (31 Dec. 2013), pp.1-6, 6 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2013-08-31
Country of Publication
Egypt
No. of Pages
6
Main Subjects
Abstract EN
Departing from the original postulates that defined various neurodegenerative disorders, accumulating evidence supports a major role for soluble forms of amyloid proteins as initiator toxins in Alzheimer’s disease, Parkinson’s disease, frontotemporal dementias, and prion diseases.
Soluble multimeric assemblies of amyloid-β, tau, α-synuclein, and the prion protein are generally englobed under the term oligomers.
Due to their biophysical properties, soluble amyloid oligomers can adopt multiple conformations and sizes that potentially confer differential biological activities.
Therein lies the problem: with sporadic knowledge and limited tools to identify, characterize, and study amyloid oligomers, how can we solve the enigma of their respective role(s) in the pathogenesis of neurodegenerative disorders? To further our understanding of these devastating diseases, the code of the amyloid oligomers must be broken.
American Psychological Association (APA)
Lesné, Sylvain E.. 2013. Breaking the Code of Amyloid-β Oligomers. International Journal of Cell Biology،Vol. 2013, no. 2013, pp.1-6.
https://search.emarefa.net/detail/BIM-510778
Modern Language Association (MLA)
Lesné, Sylvain E.. Breaking the Code of Amyloid-β Oligomers. International Journal of Cell Biology No. 2013 (2013), pp.1-6.
https://search.emarefa.net/detail/BIM-510778
American Medical Association (AMA)
Lesné, Sylvain E.. Breaking the Code of Amyloid-β Oligomers. International Journal of Cell Biology. 2013. Vol. 2013, no. 2013, pp.1-6.
https://search.emarefa.net/detail/BIM-510778
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-510778