Figure 7
Schematic overview of age-dependent BAY-induced changes in metabolite levels. (a) Crosstalk of metabolic pathways linked to altered levels of identified metabolites. Detected metabolites are bolded. Metabolites showing statistically significant changes with aging or after BAY-treatment are classified into three general pathways: energy pathways (green-framed boxes), signaling pathways (blue-framed boxes), lipid pathways (brown-framed boxes), and others (pink-framed boxes). Additionally, these metabolites are assigned to brain structures in which they titers changed in: 1 – Y-CTR vs. Y-BAY, 2 – O-CTR vs. O-BAY, 3- Y-CTR vs. O-CTR, and 4 – Y-CTR vs. O-BAY; H – hippocampus, C – cortex, Ce – cerebellum (for example: 1H means that a given metabolite changes significantly in Y-CTR in comparison to Y-BAY in the hippocampus). The remaining abbreviations: Chop – O-phosphocholine, DNPB – De Novo Purine Nucleotide Biosynthesis Pathway, G6P – Glucose-6-phosphate, PPP – Pentose Phosphate Pathway, PRPP – 5-phosphoribosyl-1-pyrophosphate, R5P – Ribose-5-phosphate, 3PGA – 3-Phosphoglyceric acid, PEA – O-phosphoethanolamine. The red “x” indicates the blockade of glycogenolysis by BAY U6751. Metabolites of various pathways origins (NAD+, pyridoxine, and ascorbate) are not included in the scheme. (b) The metabolomic fingerprint of age-dependent influence of BAY on young and old animals, in the context of changes of spatial memory formation in hippocampus. Const. indicates lack of changes; arrows mark an increase or decrease in metabolite titers.
