1. Ageing is associated with persistent pro-inflammatory responses that contribute to various health conditions, including cognitive decline and Alzheimer's disease.
2. In ageing mice, myeloid cell bioenergetics are suppressed due to increased signalling by prostaglandin E2 (PGE2), leading to reduced glucose flux and mitochondrial respiration.
3. Inhibition of myeloid EP2 signalling in aged mice rejuvenates cellular bioenergetics, reduces inflammation, improves synaptic plasticity and spatial memory, suggesting that cognitive ageing can be reversed by restoring youthful immune functions through reprogramming myeloid glucose metabolism.