Measuring Memory in a Mouse Model of Alzheimer's Disease

摘要

K. Hsiao et al. (1) describe evidence of a memory deficit that is correlated with an elevation in amyloid-containing plaques in a transgenic mouse that overexpresses the so-called Swedish mutation of amyloid precursor protein. This comment questions whether the evidence actually shows such a memory deficit. First, although the performance of the transgenic mice was impaired, they did show signs of learning. Figure 2E in the report demonstrates that the 9- to 10-month-old transgenic mice performed more poorly than did wild-type mice in the visible platform subtest of the Morris water maze, a result which is usually taken to indicate a sensory-motor impairment, not a memory deficit. On two of the four individual days of the subtest, such differences were statistically significant; but it is not shown whether an overall analysis would also produce a significant result. In the absence of basic measures of locomotor activity, vegetative functions, or sensory capacity, perhaps these 9- to 10-month-old animals are sluggish. By the fourth block of trials, the transgenic mice improved, although they remained significantly slower than controls.