Fig. 3.

Knockout of the CatB gene, but not BACE1, in AβPPWT/Lon mice improves memory deficits. Memory deficits of AβPPWT/Lon mice were assessed 2 days after completion of the training in the Morris water maze test by measuring the latency period (Panel A) and distance traveled (Panel B) for animals to swim to the submerged, invisible platform. The shorter latency periods and shorter distances traveled indicate improved memory. AβPPWT/Lon (control), AβPPWT/Lon × CatB KO (CatB KO), and AβPPWT/Lon × BACE1 KO (BACE1 KO) mice had mean latency periods of 39, 16, and 37 seconds, respectively (Panel A), and mean distances traveled of 194, 114, and 195 cm, respectively (Panel B). Memory function of normal non-transgenic wild-type mice of the same strain and age is shown by the dotted line, of 14 seconds latency (Panel A) as reported previously [7]. Values are expressed as x ± s.e.m., and n = 10 per group. ***Statistically significant (p < 0.05).