= −0.08, t = 239, P<0.05) (Figures 4c and d), but did not differ from other cohort members on Aggression (β = −0.04, t = 1.31, P>0.05) or Alienation (β = −0.05, t = 1.64, P>0.05). Thus, FAAH genetic variation was associated with individual differences in specific fear-related traits. While these human genetic associations of FAAH with stress-reactive personality and habituation of amygdala-mediated threat responses await replication, they provide clear convergence with our rodent data showing that FAAH inhibition facilitates amygdala-mediated fear extinction. Among the key avenues for future studies will be a test of whether FAAH variation associates specifically with human fear extinction and prevalence of extinction-impaired neuropsychiatric disorders such as post-traumatic stress disorder.
