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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer’s disease mutations but not by inhibition of BACE1

Fig. 1

APP and APP C-terminal fragment levels. a–g Cortical (a, c, e, g) and hippocampal (a, b, d, f) levels of full-length (FL) APP and APP C-terminal fragments (CTFs) were determined in 6–8-month-old genetically modified mice (+) and WT controls (−) from the indicated lines by western blot analysis with antibodies 22C11 (epitope: amino acids 66–81 of the APP N-terminus) and CT15 (epitope: amino acids 680–695 of the APP C-terminus). a Western blot depicting bands representing APP holoprotein, C99 (also known as β-CTF), and C83. Actin-α1 was used as a loading control. b–g Quantitations of relative APP (b, c), C99 (d, e), and C83 (f, g) levels. The same set of J20 standards was included in each blot to normalize signals across blots as described in Materials and Methods. n = 5–15 mice per group. *P < 0.05, **P < 0.01, ***P < 0.01, **** P < 0.0001 vs. WT from same line or as indicated by brackets, based on multiple Welch t-test (b, d–f) or permutation test (c, g), with Holm-Sidak correction. Values are means ± SEM

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Molecular Neurodegeneration

ISSN: 1750-1326