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Bridging the gap: From protein misfolding to protein misfolding diseases

期刊

FEBS LETTERS
卷 583, 期 16, 页码 2581-2586

出版社

WILEY
DOI: 10.1016/j.febslet.2009.06.030

关键词

Amyloid; Neurodegeneration; Nanoscience; D. melanogaster; C. elegans

资金

  1. Wellcome Trust
  2. Medical Research Council
  3. MRC [G0700990] Funding Source: UKRI
  4. Medical Research Council [G0700990] Funding Source: researchfish

向作者/读者索取更多资源

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. (C) 2009 Published by Elsevier B. V. on behalf of the Federation of European Biochemical Societies.

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