Interplay between Wnt signaling and other anti-ageing pathways. In this scheme we show the integration and interaction of multiple signaling pathways: the first line (top) shows a Wnt ligand, binding Frizzled receptor and activated canonical and non-canonical Wnt signaling. The canonical pathway (left) leads to GSK3β inhibition. AMPK activation is known to inhibit by GSK3β. The non-canonical pathway (right) increases intracellular Ca2+ levels. Nitric oxide (NO), a second messenger, is known to directly activate AMPK. AMPK is also activated by Ca2+ through CaMKK2. Therefore, AMPK activation by the Wnt pathway represents a hypothetical concept (“theoretical model” in transparent gray box). In the second line, AMPK leads to activation of Sirt1 (right). Sirt1 de-acetylates PGC-1α, and this transcription factor translocates to the nucleus and interacts with PPARγ heterodimerization to enhance the expression of mitochondrial biogenesis genes. As well, AMPK inhibits mTOR complex (right) resulting in autophagy stimulation. Additionally, we show the established target of several compounds (Li+, Metformin, Rapamicin, Resveratrol and Thiazolidinediones) on these intricate inter-linking signaling pathways to neuronal energy availability and cellular life span. Abbreviations: G, G-protein-coupled receptor; Dvl, Segment polarity protein disheveled homolog DVL-1; APC, adenomatous polyposis coli protein; Ca2+, calcium; Ca2+/CaM-dependent protein kinase kinase β (CaMKKβ); AMPK, 5' adenosine monophosphate-activated protein kinase; mTOR, mechanistic target of rapamycin, Sirt1, silent mating-type information regulator 2 homolog 1; PGC-1α, peroxisome proliferator-activated receptor gamma co-activator 1-α; GSK-3β, Glycogen synthase kinase 3; P,PPARα, phosphorylation; peroxisome proliferator-activated receptor alpha; Li+; lithium.