Abstract
Protein misfolding and aggregation are pathognomic for a number of the most common age‐related degenerative diseases. Great progress has been made in studying protein aggregation in the test tube and also in replicating protein aggregation in vertebrate animal models of these diseases. However, we argue here that the development and effective integration of emerging techniques such as the methods of nanoscience and the use of invertebrate models are now providing powerful new opportunities to advance our current understanding of the fundamental origins of these disorders.
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Dates
Type | When |
---|---|
Created | 16 years, 2 months ago (June 22, 2009, 5:19 a.m.) |
Deposited | 1 year, 11 months ago (Sept. 18, 2023, 8:03 a.m.) |
Indexed | 2 months ago (June 24, 2025, 12:07 p.m.) |
Issued | 16 years, 2 months ago (June 21, 2009) |
Published | 16 years, 2 months ago (June 21, 2009) |
Published Online | 16 years, 2 months ago (June 21, 2009) |
Published Print | 16 years ago (Aug. 20, 2009) |
@article{Luheshi_2009, title={Bridging the gap: From protein misfolding to protein misfolding diseases}, volume={583}, ISSN={1873-3468}, url={http://dx.doi.org/10.1016/j.febslet.2009.06.030}, DOI={10.1016/j.febslet.2009.06.030}, number={16}, journal={FEBS Letters}, publisher={Wiley}, author={Luheshi, Leila M. and Dobson, Christopher M.}, year={2009}, month=jun, pages={2581–2586} }