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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Downregulating ANP32A rescues synapse and memory loss via chromatin remodeling in Alzheimer model

Fig. 1

ANP32A elevation is correlated with learning deficit in htau mice. a–c Only the 12 m- but not 4 m- and 8 m-old htau transgenic mice show increased latency during 6 days learning trials in MWM test when compared with the age-matched wild-type (wt) littermates (a: wt, n=10, htau, n=9; b: wt, n=15, htau, n=12; c: n=9 each group). Data were presented as mean ± s.e.m. *, p<0.05, **, p<0.01 vs wt (one-way repeated measures ANOVA and Bonferroni’ s post hoc test). d–i Only the 12 m- but not 4 m- and 8 m-old htau mice show increased ANP32A level in cortex (Cr) and hippocampus (Hip) compared with the wt littermates, and no difference of ANP32A was detected in cerebellum (Cb) measured by Western blotting. Tubulin probed by DM1A was used as a loading control. Data were presented as mean ± SD. **, p<0.01 vs wt (Unpaired Student's t-test (two-tailed)). j The representative images of ANP32A in hippocampus measured by immunohistochemical staining (n=3-6 slices from 3 mice for each group)

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