Clinicians and researchers teamed up to investigate how inappropriate proinflammatory mechanisms contribute to the pathogenesis of drug-refractory epilepsy.
In mice, epigenetic marks made on histones during infancy influence depression-like behavior during adulthood. A drug that reverses the genomic tags appears to undo the damage.
Knocking out the receptor for a lipid that causes inflammation rejuvenates macrophage metabolism and restores cognitive function in an Alzheimer’s disease model.