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2-180 - From early-life adversity to psychopathology: discovering distinct trajectories, latent vulnerabilities and protective factors

Fri, April 7, 2:15 to 3:45pm, Austin Convention Center, Meeting Room 18B

Session Type: Paper Symposium

Integrative Statement

Exposure to early-life stress powerfully predicts disabling and costly adult mental health conditions. While this link is well-established there is poorer understanding of the intermediate, precursory mechanisms that translate these risks. These mechanisms could lie ‘latent’ until later events precipitate symptoms (McCrory & Viding, 2015), or they may never be expressed in individuals ‘protected’ from negative outcomes. A new model (McLaughlin, 2015) further suggests that EAs may show distinctive features such as ‘threat’ or ‘deprivation’, and leave subtly different marks on the developing brain and information-processing but these hypotheses require empirical validation. This multidisciplinary symposium addresses questions relating to the intermediate mechanisms between EA and psychopathology, potential protective factors and distinct trajectories between different types of EA. The first three talks will present data on linkages between childhood maltreatment and cognitive functioning, and discuss whether these variables could reflect latent vulnerability factors. The first talk additionally highlights the protective effect of resting vagal tone (a physiological marker of neural flexibility) in moderating associations between maltreatment and psychopathology. The second talk suggests that there are also differences at the neural processing of affective information. The third talk further suggests that the experience of threat versus deprivation in early-life could be associated with distinct sets of latent vulnerability markers. Capitalising on the findings of the previous talks, the fourth talk presents data on the epigenetic signature of EAs, showing that exposure to various EAs can impact methylation patterns around certain genetic loci, and that distinct EA can have distinct biological signatures.

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