Beta Amyloid Peptide: Research Paper : Metabolic reprogramming rejuvenates aged myeloid cells restoring cognition

Metabolic reprogramming rejuvenates aged myeloid cells restoring cognition

Abstract

Inflammaging is associated with aging-associated cognitive loss and neurodegeneration. Chronic NSAID use has been reported to reduce the incidence of Alzheimer's Disease (AD), presumably by inhibiting inflammation, although NSAIDs appear to not be good candidates for anti-AD therapeutics given disappointing clinical trial results. Prostaglandin E2 (PGE2) acts downstream of NSAID target COX-2, a cyclooxygenase, to activate several G-protein coupled receptors (GPCR) including EP2, which is now reported to reduce glycolysis and oxidative phosphorylation during aging by increasing glycogen synthesis and polarizing myeloid cells toward the M1 pro-inflammatory phenotype. Inhibiting EP2 using small molecule drugs, polarizes macrophages toward the anti-inflammatory phenotype, restores youthful metabolism and mitochondrial morphology as well as youthful hippocampus-based memory capability. EP2 may be a better target than cyclooxygenases for the development of drugs that improve age-associated mild cognitive impairment and possibly even for the development of drugs to treat dementias.

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