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Aβ delays fibrin clot lysis by altering fibrin structure and attenuating plasminogen binding to fibrin
Alzheimer disease is characterized by the presence of increased levels of the β-amyloid peptide (Aβ) in the brain parenchyma and cerebral blood vessels. This accumulated Aβ can bind to fibrin(ogen) and render fibrin clots more resistant to degradation. Here, we demonstrate that Aβ(42) specifically b...
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| Hlavní autoři: | , |
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| Médium: | Artigo |
| Jazyk: | Inglês |
| Vydáno: |
American Society of Hematology
2012
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| Témata: | |
| On-line přístup: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3321860/ https://ncbi.nlm.nih.gov/pubmed/22238323 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1182/blood-2011-11-389668 |
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