Drug blocks stress-response protein, preventing mouse social deficits from early hardship

Researchers in Munich and Stockholm simulated early-life stress in mice by depriving mother rodents of adequate bedding, leading to erratic maternal care and unpredictable infancy. Although the affected mice showed no outward illness, they consistently fell to the lowest tiers of social groups as adolescents and adults. Administration of SAFit2, a compound that inhibits the protein FKBP51, to the mothers during the stressful phase prevented these social deficits, with treated offspring matching the performance of mice raised under normal conditions.

Brain analysis indicated that the drug reversed widespread gene-activity alterations, especially in the medial prefrontal cortex and nucleus accumbens, areas linked to emotion and reward. The study, published in June, demonstrates that blocking FKBP51 can prevent the lasting impact of early adversity, but it does not prove reversal after trauma has occurred, and the drug is not yet ready for human use.