Part II | Vascular risk factors for depression and apathy 147 8 life depression and once again these findings link late-life depression in low neurotic populations to cerebrovascular disease 11. Not part of this thesis, but quite relevant for the interpretation of these results is another study 12 in which our group explored the interplay between subclinical atherosclerotic disease and neuroticism in the prediction of late-life depression in 50-70 year-old participants of theNijmegen Biomedical Study. A principal component analysis of scores on the Beck Depression Inventory yielded two factors, one representing a cognitive-affective symptom cluster and the other a somatic-affective symptom cluster. Atherosclerotic disease as measured by the intima media thickness of the carotid arteries was only associated with the somatic-affective symptom cluster, where severe atherosclerosis attenuated the association between neuroticism and cognitive-depressive symptoms. This latter finding replicated the results of our earlier study (Chapter 4) and provided more substantial support for the hypothesis that the negative interaction between neuroticism and vascular disease in the prediction of depression might be explained by apathy due to cerebrovascular disease. An imaging study of older individuals with depression showed that white matter hyperintensities (WMH) and lacunar infarcts - as biomarkers of cerebral small vessel disease- were mainly associated with symptoms of anhedonia, concentration problems, psychomotor retardation, appetite disturbance and motivational problems 13. When the depressive symptom profiles of three different biological pathways to late-life depression, more specifically vascular disease, inflammation and neurodegeneration, were considered, vascular disease was associated with motivational problems, psychomotor retardation and loss of energy 14. All of these symptoms were not exclusively associated with vascular disease, however, and could also be a consequence of inflammation (loss of energy) or neurodegeneration (motivational problems, psychomotor retardation) 14. Together these findings highlight the complexity of the interplay of late-life depression, cerebrovascular disease and other major risk-factors. First, the relationship between cerebrovascular disease and depression might be reciprocal but could also be partly explained by residual confounding in that atherosclerotic disease of the cerebral small vessels might enhance the risk of both depression and stroke (Chapters 2 and 3). Furthermore, in certain populations the vascular pathway to depression might be more prominent and thus more easily detected, while in other populations, such as those characterized by high neuroticism, the vascular route to depression might be slighter or (largely) obscure by interaction effects or due to overshadowing by more important risk factors (Chapters 2,3 and 4). Different aetiological pathways to depression might exert differential effects on the brain morphology and functioning 11. The vascular pathway is then associated with a specific, although not exclusive, depressive symptom profile, with motivational problems and psychomotor retardation 12 13 14, representing the depressiveexecutive subtype of depression 15.
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