Glycolysis‐derived L‐serine in hippocampal astrocytes rescues synaptic plasticity and memory loss in a mouse model of Alzheimer’s disease

Impairment of glycolysis has often been observed early in the course of Alzheimer’s disease, although it is not known whether this deregulation contributes to the cognitive deficits observed in the disease. Aside from ATP production, a major function of glycolysis is to provide precursors, such as L‐serine, to support macromolecular synthesis. L‐serine is a metabolic hub and plays pivotal role in the brain. It is the precursor of D‐serine, the principal co‐agonist of synaptic N‐methyl D‐aspartate receptors (NMDARs) required for the induction of long‐term synaptic plasticity in the hippocampus. It also contributes to the homeostasis of synapses and of mitochondrial function by providing lipids.