Direct measurement of lipid membrane disruption connects kinetics and toxicity of Aβ42 aggregation
(2020) In Nature Structural and Molecular Biology 27(10). p.886-891- Abstract
The formation of amyloid deposits in human tissues is a defining feature of more than 50 medical disorders, including Alzheimer’s disease. Strong genetic and histological evidence links these conditions to the process of protein aggregation, yet it has remained challenging to identify a definitive connection between aggregation and pathogenicity. Using time-resolved fluorescence microscopy of individual synthetic vesicles, we show for the Aβ42 peptide implicated in Alzheimer’s disease that the disruption of lipid bilayers correlates linearly with the time course of the levels of transient oligomers generated through secondary nucleation. These findings indicate a specific role of oligomers generated through the catalytic action of... (More)
The formation of amyloid deposits in human tissues is a defining feature of more than 50 medical disorders, including Alzheimer’s disease. Strong genetic and histological evidence links these conditions to the process of protein aggregation, yet it has remained challenging to identify a definitive connection between aggregation and pathogenicity. Using time-resolved fluorescence microscopy of individual synthetic vesicles, we show for the Aβ42 peptide implicated in Alzheimer’s disease that the disruption of lipid bilayers correlates linearly with the time course of the levels of transient oligomers generated through secondary nucleation. These findings indicate a specific role of oligomers generated through the catalytic action of fibrillar species during the protein aggregation process in driving deleterious biological function and establish a direct causative connection between amyloid formation and its pathological effects.
(Less)
- author
- organization
- publishing date
- 2020-10
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Nature Structural and Molecular Biology
- volume
- 27
- issue
- 10
- pages
- 6 pages
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:85089256120
- pmid:32778821
- ISSN
- 1545-9993
- DOI
- 10.1038/s41594-020-0471-z
- language
- English
- LU publication?
- yes
- id
- 449d1dc4-cfd8-4fec-9dd5-4f73705033e8
- date added to LUP
- 2020-08-20 08:45:42
- date last changed
- 2024-11-28 13:25:43
@article{449d1dc4-cfd8-4fec-9dd5-4f73705033e8, abstract = {{<p>The formation of amyloid deposits in human tissues is a defining feature of more than 50 medical disorders, including Alzheimer’s disease. Strong genetic and histological evidence links these conditions to the process of protein aggregation, yet it has remained challenging to identify a definitive connection between aggregation and pathogenicity. Using time-resolved fluorescence microscopy of individual synthetic vesicles, we show for the Aβ42 peptide implicated in Alzheimer’s disease that the disruption of lipid bilayers correlates linearly with the time course of the levels of transient oligomers generated through secondary nucleation. These findings indicate a specific role of oligomers generated through the catalytic action of fibrillar species during the protein aggregation process in driving deleterious biological function and establish a direct causative connection between amyloid formation and its pathological effects.</p>}}, author = {{Flagmeier, Patrick and De, Suman and Michaels, Thomas C.T. and Yang, Xiaoting and Dear, Alexander J. and Emanuelsson, Cecilia and Vendruscolo, Michele and Linse, Sara and Klenerman, David and Knowles, Tuomas P.J. and Dobson, Christopher M.}}, issn = {{1545-9993}}, language = {{eng}}, number = {{10}}, pages = {{886--891}}, publisher = {{Nature Publishing Group}}, series = {{Nature Structural and Molecular Biology}}, title = {{Direct measurement of lipid membrane disruption connects kinetics and toxicity of Aβ42 aggregation}}, url = {{http://dx.doi.org/10.1038/s41594-020-0471-z}}, doi = {{10.1038/s41594-020-0471-z}}, volume = {{27}}, year = {{2020}}, }