ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Pharmacological Inhibition of FKBP51 Mitigates Early Life Adversity-Induced Social Deficits in Male Mice.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Social hierarchy shapes behavioral and transcriptional responses to chronic stress and ketamine in male mice.iScience · 2026Article
- Pharmacological Inhibition of FKBP51 Mitigates Early Life Adversity-Induced Social Deficits in Male Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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16 authors.
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Abstract
Early life adversity (ELA) is a major risk factor for psychiatric disorders, but targeted preventative strategies are lacking due to poor mechanistic insight. The FKBP51 protein, a co-chaperone of the glucocorticoid receptor, is a key mediator of stress vulnerability. We tested if pharmacological inhibition of FKBP51 with the selective inhibitor SAFit2 prevents the long-term consequences of ELA. Male mice exposed to ELA exhibited persistent deficits in social behavior, manifesting as social subordination in adolescence and adulthood. Early-life SAFit2 treatment fully rescued these ELA-induced behavioral impairments. Transcriptional profiling across six stress-relevant brain regions revealed that SAFit2 normalized ELA-driven gene expression changes, particularly in the medial prefrontal cortex and nucleus accumbens. Functional analysis showed the rescue converged on immunoregulatory and neuroactive ligand-receptor signaling pathways. Our findings establish FKBP51 as a critical pharmacological target for reversing the lasting impact of early life adversity on brain function, offering a path toward preventative treatment for ELA-related psychopathology.
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