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. 2016 Mar 10;12(5):784–800. doi: 10.1080/15548627.2016.1159375

Figure 8.

Figure 8.

Decreased enzymatic activity and protein levels of IDE in the CSF of patients with AD. (A) IDE enzymatic activities in the CSF of control subjects and patients with AD (N = 10 in each group). RFU, relative fluorescence unit. (B) IDE activity data from the CSF show a correlation with the MMSE score (r = 0.4657, P value = 0.0385). (C) IDE activities in the CSF of AD patients show a tendency of negative correlation with AD group CDR scores (r = −0.0809, P = 0.4120). (D) Gender difference in IDE enzymatic activities. (E) IDE expression levels in the CSF of control subjects and patients with AD (N = 10 in each group). (F) The levels of IDE proteins in the CSF correlate with the MMSE score (r = 0.5155, P value = 0.0200). (G) Like IDE activity, IDE protein levels in the CSF of AD patients show a negative correlation with CDR scores calculated in the AD groups (r = −0.4042, P = 0.2467). (H) Gender difference in IDE levels in the CSF. Values are mean ± SEM *, P < 0.05; **, P < 0.01. ‘n.s.’ means not significant. (I) Schematic diagram of this study. Aβ increases IDE secretion from astrocytes via an autophagy-based unconventional secretory pathway, and Aβ-induced IDE secretion depends on the activity of RAB8A and GORASP. In the AD brain, lysosomal dysfunction occurs and, as a result, Aβ-induced IDE secretion is inhibited because autophagic flux is important for IDE secretion. Reduced IDE levels may result in increased levels of extracellular Aβ and contribute to the progression of AD pathogenesis.