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Fig. 3 | Alzheimer's Research & Therapy

Fig. 3

From: The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model

Fig. 3

SynGO analyses of synaptic protein regulation by SUL-138 in APP/PS1 and wildtype mice. A Differential synaptic protein expression was determined for three contrasts, APP VEH vs. WT VEH (blue), APP SUL vs. APP VEH (purple), and WT SUL vs. WT VEH (orange), resulting in the indicated numbers of significant differentially expressed proteins (FDR, q ≤ 0.05). B Sunburst plots of CC enrichment for significantly downregulated proteins in APP VEH vs. WT VEH using SynGO showing significant enrichment of multiple pre- and post-synaptic GO terms. Upregulated proteins were annotated to the presynaptic endocytic zone and to synaptic vesicles. C Sunburst plots of CC enrichment for significantly downregulated proteins in APP SUL vs. APP VEH reveals modest enrichment for proteins belonging to the pre- and postsynaptic membrane and presynaptic cytosol. Upregulated proteins show a significant enrichment for postsynaptic intermediate filament (IF) and actin cytoskeleton proteins. D Sunburst plots of CC enrichment for significantly down- and upregulated proteins in WT SUL vs. WT VEH do not show any specific enrichment of synaptic GO terms

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