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. Author manuscript; available in PMC: 2019 Apr 29.
Published in final edited form as: J Alzheimers Dis. 2018;66(3):971–981. doi: 10.3233/JAD-180302

Fig. 2.

Fig. 2.

Plasma NDE concentrations of Aβ1-42, NRGN, synaptophysin, synaptotagmin, and synaptopodin are not modulated with GHRH treatment while plasma NDE concentrations of p-tauS396 and GAP43 are not modulated by cognitive status or GHRH treatment. Plasma NDE concentrations for Aβ1-42 (A) were increased while plasma NDE concentrations for NRGN (B), synaptophysin (C), synaptotagmin (D), and synaptopodin (E) were significantly reduced in MCI patients as compared to CNC patients, independent of GHRH treatment. Plasma NDE concentrations for ptau-S396 (F) and GAP43 (G) were not significantly different between both patient groups (CNC versus MCI), independent of GHRH treatment. There was no significant difference in plasma NDE concentrations for all biomarkers (A-G) in placebo-treated, MCI patients as compared to GHRH-treated, MCI patients. 1-way ANOVA with Tukey’s multiple comparisons post-hoc test; *p < 0.05 versus placebo-treated, CNC, **p < 0.01 versus GHRH-treated, CNC.