Abstract
Deposition of extracellular amyloid-β (Aβ) aggregates in the brain is one of the prime hallmarks in Alzheimer disease (AD). While high molecular weight Aβ plaques are observed in post-mortem AD brains, low-molecular weight, soluble Aβ oligomers are the primary toxic agents. Formation of these Aβ oligomers can be catalyzed by several interacting partners such as metal ions, other proteins, and lipids. We have previously demonstrated the generation of conformationally distinct oligomers of Aβ in the presence of lipid micelles.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
