Vascular risk factors for depression and apathy | Part II 146 Do neuroticism and vascular disease interact in the risk of depression, or in depressed populations in the risk of stroke? In the research presented in Chapters 3 and 4 we explored interactions between neuroticism and vascular disease in the prediction of stroke and depression. In Chapter 3, we hypothesized that the relationship between depression and strokewas based on residual confounding, with generalized atherosclerosis both forming a risk factor for depression as well as for stroke and thus that the association between depression and stroke would be stronger in vascular disease-related depression than it would be in neurotic depression. We examined the influence of low neuroticism and the presence of vascular disease on the relationship between depression and stroke in the LASA population (N=2050) during 9 years of follow-up. The incidence of stroke was determined based on self-report data, data from general practitioners and death certificates. Neuroticism was assessed using the Dutch Personality Questionnaire and depression using the CES-D. Among participants with a history of cardiac disease (N=1649) depression predicted stroke independent of the level of neuroticism (HR: 1.05, 95% CI: 1.01-1.10), whereas in the group without pre-existent cardiac disease depression predicted incident stroke only in individuals with low neuroticism (HR 1.05, 95%: 1.00-1.09) and not in those with high neuroticism. We accordingly suggested that late-life depression in context of low neuroticism is a marker of CSVD. In the Nijmegen Biomedical Study, a population-based survey conducted between 2002 and 2005 reported in Chapter 4, we looked at the interplay between vascular disease and neuroticism in the prediction of late-life depression in participants (N=1396) aged 70 and over. As neuroticism enhances the impact of life-events and has been linked to a worse adherence to (vascular) treatment, we hypothesized a positive interaction in which high neuroticism would increase the effect of vascular disease on the risk of depression. Depression was assessed using the CES-D and the level of neuroticism (0-12) was measured by means of the Eysenck Personality Questionnaire. Vascular disease was categorized into four levels based on their relatedness to brain damage, i.e., nonvascular disease or a single risk factor, two or more vascular risk factors without vascular disease, the presence of cardiac disease, and finally, the presence of stroke. The results were different for men and women. In the female respondents neuroticism was a strong predictor of depression (OR: 1.6, 95% CI: 1.4-1.8), while in their male counterparts both cardiac disease and stroke attenuated the predictive value of neuroticism (cardiac disease by neuroticism: OR: 0.8, 95% CI: 0.6-0.9; stroke by neuroticism: OR: 0.8, 95% CI: 0.6-0.96). We suggested that apathy caused by vascular disease might attenuate the effect of neuroticism on the risk of depression. A recent study of the neurobiological basis of neuroticism in late-life depression provides these results with more context: compared to findings for neurotic, depressed individuals, in non-neurotic peers a higher volume of non-white matter hypointensities was observed on T1-weighted images, which hypointensities are possibly related to cerebrovascular disease, while frontal volumes were smaller in those with high-level neuroticism. These results suggest that different neural pathways may be involved in different types of late-
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