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An Intracellular Threonine of Amyloid-β Precursor Protein Mediates Synaptic Plasticity Deficits and Memory Loss

Figure 2

A Thr668Ala mutation on APP prevents the short-term memory deficit of FDDKI mice.

(a and b) In RAWM testing, FDDKI/APPTA/TA, FDDKI/APPTA/WT, APPTA/TA, APPTA/WT mice made the same number of errors as WT mice at both 5.5 months and 9 months of age. At 5.5 months of age, FDDKI mice made significantly more errors at A4 (versus FDDKI/APPTA/TA P = 0.0007; versus FDDKI/APPTA/WT P = 0.0028; versus WT P = 0.0005) and R (versus FDDKI/APPTA/TA P = 0.0017; versus FDDKI/APPTA/WT P = 0.0005; versus WT P = 0.0005) (a). Similar results are found at 9 months of age; FDDKI mice made significantly more errors at A4 (versus FDDKI/APPTA/TA P = 0.0004; versus FDDKI/APPTA/WT P = 0.019; versus WT P = 0.0003) and R (versus FDDKI/APPTA/TA P = 0.0006; versus FDDKI/APPTA/WT P = 0.004; versus WT P<0.0001). Thus, the APPTA/TA and APPTA/WT point mutations prevent the development of working memory deficits in FDDKI mice (b). (c and d) WT, FDDKI, FDDKI/APPTA/TA, FDDKI/APPTA/WT, APPTA/TA and APPTA/WT mice have similar speed (c) and need similar time (d) to reach a visible platform.

Figure 2

doi: https://doi.org/10.1371/journal.pone.0057120.g002