Vascular risk factors for depression and apathy | Part II 110 Alzheimer’s disease 56 57 58. In the frontal regions, the temporal regions, and the anterior cingulate, all areas which have been studied specifically, cortical thinning could be caused by aging as well as Alzheimer’s disease. Our review has shown that associations in the general population between apathy and the WMH-related regions of cortical thinning (parietal lobes, anterior insula and caudate nuclei) have not been studied yet. This is a consideration for future research, more than it is a counterargument for an association between SSVD and apathy. The vascular apathy hypothesis and the vascular depression hypothesis Depression can be a confounder when looking for the relationship between vascular disease and apathy, since apathy may be a symptom of depression (anhedonia), while it has also been related to vascular disease 25 59. Of the fourteen studies we reviewed, twelve controlled for depression 9 29 30 31 32 43 44 45 47 49 50 51. In three of these latter studies the GDS was used as a measure of both apathy and depression 9 29 44 and in five articles 31 32 47 49 50 the GDS was used as a measure of depression, including the three apathy items of this scale. Since these GDS apathy items show a low sensitivity and a high specificity as a measure of apathy in older populations 38 correction for depression measured by the GDS may imply that apathy was also corrected for, attenuating the SSVD-apathy association. If depression was overcorrected for in these studies, the associations between SSVD and apathy may also have been stronger than the statistics now show. On the other hand the role of apathy in the vascular depression hypothesis is often not accounted for in research while it may potentially act as a confounder. In patients with clinical SVD, apathy was associated with reduced white matter integrity, while depression was not, when apathy was controlled for 19 21. Arguably, with the emerging evidence for the vascular apathy hypothesis one may wonder whether in research of the vascular depression hypothesis apathy was and is adequately corrected for. Limitations: As stated, most of the research we reviewed was cross-sectional, preventing us from establishing whether SSVD precedes apathy, while we were also unable to determine whether more SSVD leads to higher levels of apathy. An alternative explanation for an apathy-SSVD or an SSVD-apathy relationship in cross-sectional designs is that apathy leads to poorer cardiovascular outcomes due to differences in health behaviours 14. Does an association between CVRF and apathy then reflect the concept of vascular apathy our does it (partially) reflect differences in health behaviours that are caused by apathy? Nevertheless, the findings of an increase in the incidence of apathy with more cardiovascular pathologies 29 points towards CVRF as an aetiological factor in apathy (and not only the reverse mechanism).
RkJQdWJsaXNoZXIy MjY0ODMw