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Knock-In of Human BACE1 Cleaves Murine APP and Reiterates Alzheimer-like Phenotypes
Key neuropathological hallmarks of Alzheimer's disease (AD) are elevated levels of amyloid β-peptide (Aβ) species generated via amyloid precursor protein (APP) endoproteolysis and cleavage by the rate-limiting β-site enzyme 1 (BACE1). Because rodents do not develop amyloid pathologies, we here...
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| Main Authors: | , , , , , , |
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| Formáid: | Artigo |
| Teanga: | Inglês |
| Foilsithe: |
Society for Neuroscience
2014
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| Ábhair: | |
| Rochtain Ar Líne: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4122804/ https://ncbi.nlm.nih.gov/pubmed/25100603 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1523/JNEUROSCI.0433-14.2014 |
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