Do personality traits contribute to resiliency to brain pathology?

1. Do personality traits contribute to resiliency to brain pathology? Sarah Tomaszewski Farias, Maritza Dowling, Dan Mungas, Bruce Reed, Joshua Sonnen, Milton Strauss

2. Conceptual Approach Conceptually, reserve explains deviations from the level of cognitive performance that would be expected for a given amount of brain pathology Methodological approach: we modeled reserve as residual cognition after accounting for neuropathology (and brain weight?) and then we examined variables that account for this residual Personality trait examined: Neuroticism/distress proneness/negative affectivity and trait anxiety

3. Rationale • Chronic reaction to threat triggers overactivation of the HPA axis and the release of stress hormones (i.e. glucocorticoids, particularly cortisol) • It is hypothesized that chronic exposure to cortisol increases excitatory amino acid release, resulting in neuronal injury • The hippocampus is particularly vulnerable to such effects since it has a high density of glucocorticoid receptors • Hippocampal atrophy has been associated with PTSD and other chronic psychiatric syndromes • Elevated basal cortisol is associated with hippocampal atrophy (in pts with AD) • Frontal systems (particularly anterior cingulate) have also been implicated

4. Npath 2 Npath 3 Npath 1 Cog 1 Cog2 Cog 3 Cog4 Cog5 Cog 6 Conceptual Model Education Distress Proneness Residual/ reserve Cognitive factor Cognitive Activity

5. Data Sources • Rush Memory Assessment Project (MAP) and ROS • Similar to previous studies presented

6. Distress proneness variable

7. Trait Anxiety Variable

8. Distress proneness on residual

9. Distress proneness on residual

10. Trait Anxiety on residual

11. Model with both Distress Proneness and Trait Anxiety

12. Other variables to consider • We also examined social engagement and size of social network – neither alone or in a joint model accounted for significant variance in the residual term (trend of social engagement in individual model p = .068) • It may be possible to examine physical activity – but the variable we appear to have is only ‘current’ physical activity (not retrospective ratings of earlier life activity) and variable is highly skewed

13. Remaining questions • Previous work by the Rush group suggests that distress proneness does not relate to traditional neuropathology of aging variables (amyloid, tangels, LBs, infarcts) • Other evidence suggests chronic distress may lead to nonspecific changes such as decreased dendritic arborization • Should we look at a model that does not include brain weight (which may reflect these nonspecific changes)? • Other work from the Rush group suggest that distress proneness may have differential effects on different cognitive domains (episodic memory) • Should we look separately at the residual terms for specific cognitive domains?