Mice deficient in BACE1, the Alzheimer's β-secretase, have normal phenotype and abolished β-amyloid generation

By Yi Luo, B. Bolon, S. Kahn, B. Bennett, S. Babu-Khan, P. Denis, W. Fan, H. Kha, Jianhua Zhang, Y. Gong and 6 more. Nature Neuroscience, 2001

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Alzheimer’s Disease and the β-Amyloid Peptide (2010, neutral): “The knockout of BACE1 in mice leads to a massive reduction in the levels of the downstream products of the enzyme (Aβ and CTFβ) in brain [35–37].”
An Overview of APP Processing Enzymes and Products (2010, positive): “BACE1-deficient mice lack β-secretase activity and Aβ formation in neurons (Cai et al. 2000; Roberds et al. 2001;Luo et al. 2001.”
BACE knockout mice are healthy despite lacking the primary beta-secretase activity in brain: implications for Alzheimer's disease therapeutics. (2001, background): “One group performed a thorough histopathological analysis and found no abnormalities (15).”
APP mouse models for Alzheimer's disease preclinical studies (2017, positive): “BACE1 gene knockout abrogates cerebral A b accumulation in all APP-and APP/PS-overexpressing mice tested to date (Luo et al , 2001, 2003; Ohno et al , 2004, 2007; Laird et al , 2005; McConlogue et al , 2007; Rabe et al , 2011), validating BACE1 as the major b -secretase enzyme in the brain.”
APP processing and synaptic function. (2003, neutral): “…at 40mV. Forsence of an overt phenotype in mice lacking BACE (Cai experiments measuring synaptic responses from distant uninfectedet al., 2001; Luo et al., 2001) or APP (Zheng et al., 1996) cell pairs at positions [0,0] and [x,y], the stimulation electrode was suggests that other mechanisms…”