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HIGH BLOOD PRESSURE, BUT NOT CEREBRAL AMYLOIDOSIS, IS ASSOCIATED WITH LATE-LIFE ONSET DEPRESSION IN NON-DEMENTED ELDERLY

      Background: Previous researches on the late-life onset depression (LLOD) have revealed its association with vascular risk factors, which supported vascular depression hypothesis. However, several recent studies raised the possibility of the role of cerebral amyloidosis in LLOD. We aimed to investigate the independent association of vascular risk factors and cerebral amyloidosis with the experience of LLOD.
      Methods: Twenty eight non-demented subjects who first experienced major depressive episode after age of 60 years were recruited as LLOD patients. Twenty seven non-demented elderly individuals who had no experience of major depressive episode were also included as normal control (NC) subjects. All participants received comprehensive clinical assessment including vascular risk evaluation, 11 C labeled Pittsburgh Compound B (PiB) positron emission tomography (PET), and magnetic resonance imaging (MRI).
      Results: There were no group differences in age, education level but the frequency of female participants was significantly higher in LLOD patients compared to NC subjects. Univariate group comparison demonstrated that LLOD subjects had significantly higher systolic blood pressure than NC. In contrast, no significant between-group differences were found in regard of mean cortical PiB retention, and the frequency of PiB-positive and ApoE e4 carriers. Multiple logistic regression analysis including diagnostic group (LLOD vs. NC) as a dependent variable showed that systolic blood pressure was significantly associated with LLOD diagnostic state after controlling age, education, gender, and mean cortical PiB retention as covariates. Mean cortical PiB retention did not show any significant association with LLOD state in the same regression model.
      Conclusions: The results suggest that while vascular risk, hypertension in particular, is closely related to LLOD as indicated by vascular depression hypothesis, cerebral amyloidosis per se is probably not a major contributor to LLOD.