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. 2015 Nov 27;6:8836. doi: 10.1038/ncomms9836

Figure 1. Synaptic accumulation of NCAM2 is reduced in the hippocampus of AD-affected individuals.

Figure 1

(a) Western blot analysis of homogenates and synaptosomes prepared using brain tissue from cerebellum, temporal cortex and hippocampus of control and AD individuals. Note enrichment of synaptophysin, PSD95, actin, VGLUT and VGAT in synaptosomes indicating efficient synaptosome isolation. NCAM2 is highly enriched in synaptosomes versus homogenates from the hippocampus in control but not in AD individuals. Full-length versions of the western blots are shown in Supplementary Figs 6 and 7. (b) Graphs show the ratio of the respective protein levels in synaptosomes to homogenates for individual cases and mean±s.e.m. (n=10 control and n=10 AD cases were analysed). *P=0.0039, Mann–Whitney test. (c) Western blot analysis of the soluble protein fractions and synaptosomes prepared using brain tissue from the cerebellum, temporal cortex and hippocampus of control and AD individuals. Total protein concentration in synaptosomes was kept at 25% of that in the soluble protein fraction to improve visualization of the protein bands in both fractions on one blot. Probes were analysed with antibodies against the extracellular domain of NCAM2 and GAPDH, which served as a loading control. Note increased levels of soluble ∼100-kDa NCAM2 fragments in the soluble protein fraction from the hippocampus and temporal cortex of the AD individuals. Full-length versions of the western blots are shown in Supplementary Fig. 8. (d,e) Graphs show NCAM2 levels in the soluble protein fraction normalized to NCAM2 levels in synaptosomes (d) and NCAM2 levels in the soluble protein fraction normalized to GAPDH levels in homogenates (e) for individual cases and mean±s.e.m. (n=10 control and n=10 AD cases were analysed). *P<0.05, Mann–Whitney test.