In recent genome-wide association studies, clusterin has been identified as a risk factor for AD 
. Currently available cerebrospinal fluid markers can identify prodromal AD with acceptable accuracy 
. However, plasma is easier to obtain than cerebrospinal fluid and supported by the genomic studies, studies proposing clusterin as a potential plasma marker identifying AD 
have created a large interest.
As a result, several studies have recently investigated peripheral clusterin levels both in presymptomatic and symptomatic AD. IJsselstijn et al.
showed that there was no significant difference in clusterin levels between presymptomatic AD subjects and controls 
. Two recent studies have reported increased plasma clusterin levels in AD relative to healthy controls 
. Contrastingly, two other studies found no difference in clusterin levels between healthy controls and AD patients 
. In the current study, we did not observe increased plasma levels in AD subjects compared to controls and we have found that plasma clusterin levels could not discriminate AD subjects from healthy controls, nor with subjects with other dementias.
Thambisetty and coworkers showed, in 2010, that higher concentrations of plasma clusterin were associated with greater atrophy of the entorhinal cortex in AD. By contrast, in 2012, Thambisetty and coworkers found that in mild cognitive impairment, higher plasma clusterin levels were associated with slower rates of brain atrophy 
. Our findings demonstrate no inverse correlation between clusterin levels in plasma and cognitive performance in individuals with AD, in contradiction to recent publications showing plasma clusterin to associate with both prevalence and severity of AD 
. We observed a weakly positive association between plasma clusterin and MMSE, suggesting a weakly negative association between plasma clusterin and severity of cognitive impairment.
Interestingly, in the present study, plasma clusterin levels were significantly increased in subjects with depression. Although there are no previous reports linking clusterin to depression, our finding that clusterin is increased in subjects with depression ties in with the growing evidence on inflammatory markers as potential markers for depression. Several studies consistently report that subjects with depression demonstrate increased plasma levels of a variety inflammatory biomarkers when compared with nondepressed subjects 
Interestingly, increased levels of the complement factors C3 and C4 have been observed in patients with depression compared to controls 
. It would, therefore, be interesting to investigate whether the increased clusterin levels that we observe in depressed subjects are linked to increased complement activation. Although the finding of increased plasma clusterin in depression fits in with the hypothesis of depression being an inflammatory disorder, it is necessary to replicate this finding in a different and larger cohort.