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Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer’s Disease and Down syndrome
Full-length amyloid beta peptides (Aβ(1–40/42)) form neuritic amyloid plaques in Alzheimer’s disease (AD) patients and are implicated in AD pathology. However, recent transgenic animal models cast doubt on their direct role in AD pathology. Nonamyloidogenic truncated amyloid-beta fragments (Aβ(11–42...
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| Hlavní autoři: | , , , , , , , |
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| Médium: | Artigo |
| Jazyk: | Inglês |
| Vydáno: |
National Academy of Sciences
2010
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| Témata: | |
| On-line přístup: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2851998/ https://ncbi.nlm.nih.gov/pubmed/20308552 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.0914251107 |
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