Early Life Stress and High Levels of FKBP5 Protein Heighten Anxiety-Like Behavior, Lending Support to Importance of Gene-Environment Interactions in Neuropsychiatric Disease Risk

Researchers continue to dig for molecular clues to better understand how gene-environment interactions influence neuropsychiatric disease risk and resilience. An increasing number of studies point to a strong association between the FKBP5 gene and increased susceptibility to depression, anxiety, post-traumatic stress disorder, and other mental health disorders. Adding to the growing evidence, a new preclinical study by University of South Florida (USF) neuroscientists finds that anxiety-like behavior increases when early life adversity combines with high levels of FKBP5 - a protein capable of modifying hormonal stress response. Moreover, the researchers demonstrate this genetic-early life stress interaction amplifies anxiety by selectively altering signaling of the enzyme AKT in the dorsal hippocampus, a portion of the brain primarily responsible for cognitive functions like learning and memory. While more research is required, the study suggests that FKBP5 may be an effective target for treating anxiety and other mood disorders. The findings were published online on June 4, 2019 in the International Journal of Molecular Sciences. The open-access article is titled “Early Life Stress and High FKBP5 Interact to Increase Anxiety-Like Symptoms through Altered AKT Signaling in the Dorsal Hippocampus.” "We know that the combination of genetic variations and environmental factors can make people either more or less susceptible to mental illness -- even when they experience the same types of trauma," said senior author Laura Blair, PhD, Assistant Professor of Molecular Medicine at the USF Health Byrd Alzheimer's Center. Postdoctoral scholar Marangelie Criado-Marrero, PhD, was lead author of the study.
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