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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Autori principali: Plucińska, Kaja, Crouch, Barry, Koss, David, Robinson, Lianne, Siebrecht, Michael, Riedel, Gernot, Platt, Bettina
Natura: Artigo
Lingua:Inglês
Pubblicazione: Society for Neuroscience 2014
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Accesso online: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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