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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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| Główni autorzy: | , , , , , , , |
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| Format: | Artigo |
| Język: | Inglês |
| Wydane: |
National Academy of Sciences
2010
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| Hasła przedmiotowe: | |
| Dostęp online: | 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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