A Food and Drug Administration-approved Asthma Therapeutic Agent Impacts Amyloid β in the Brain in a Transgenic Model of Alzheimer Disease

Interfering with the assembly of Amyloid beta (A beta) peptides from monomer to oligomeric species and fibrils or promoting their clearance from the brain are targets of anti-A beta-directed therapies in Alzheimer disease. Here we demonstrate that cromolyn sodium (disodium cromoglycate), a Food and Drug Administration-approved drug already in use for the treatment of asthma, efficiently inhibits the aggregation of A beta monomers into higher-order oligomers and fibrils in vitro without affecting A beta production. In vivo, the levels of soluble A beta are decreased by over 50% after only 1 week of daily intraperitoneally administered cromolyn sodium. Additional in vivo microdialysis studies also show that this compound decreases the half-life of soluble A beta in the brain. These data suggest a clear effect of a peripherally administered, Food and Drug Administration-approved medication on A beta economy, supporting further investigation of the potential long-term efficacy of cromolyn sodium in Alzheimer disease.