Our results show a positive correlation between age and protein levels in CSF (MBP, NSE, S100B) and serum (GFAP, S100B) in accordance with van Engelen et al,17
who showed a clear age dependency of MBP, NSE and S100B in CSF. However, in contrast with Rosengren et al
no significant correlation between GFAP levels and age was found. A general influence on our results was ruled out by using matched controls and including age as a covariate in the statistical analysis.
Secondly, significantly higher concentrations of S100B were found in the CSF and serum of patients with schizophrenia, confirming the results of previous studies. However, there was no indication for increased release of GFAP and MBP from damaged astrocytes and oligodendrocytes or myelin, or release of NSE due to acute neuronal loss. This may be interpreted as indirect evidence for increased active secretion of S100B in the brains of people during acute psychosis in schizophrenia. Nevertheless, it remains unclear whether increased S100B secretion plays a pathogenetic role in the context of schizophrenia or whether it must be interpreted as a compensatory attempt.19
The present constellation of findings with an isolated S100B increase in CSF and serum is dissimilar to neurodegenerative disorders. In Alzheimer's disease, for example, along with increased S100B concentrations increased GFAP and NSE were also found in the CSF, which correlated with the degree of atrophy.5,20,21
The fact that CSF findings are dissimilar to neurodegenerative diseases does not exclude the early stages of a neurodegenerative disease in our patients with first‐onset schizophrenia. However, it should be noted that histological studies on schizophrenia—in contrast with those on Alzheimer's disease—found no indications of astrogliosis or neuronal loss.22,23,24
In comparison with acute relapses in multiple sclerosis, it should be mentioned that increased MBP can be detected in the CSF and serum of patients with multiple sclerosis, owing to the destruction of myelin and oligodendrocytes.12
Although disorders of myelinisation are discussed in the context of schizophrenia, there was no evidence for an acute destruction of myelin or oligodendrocytes during acute psychotic episodes.25
The present study has certain limitations that need to be taken into account: (1) Sample sizes were small; however, our finding of increased S100B in the CSF of patients with schizophrenia was confirmed after Bonferroni correction. (2) The confounding factor of drugs cannot be ruled out with this study and has to be examined by extending the study to unmedicated patients with schizophrenia. However, our study is in accordance with that by Rothermundt et al
who also found increased S100B levels in CSF and serum of unmedicated patients with schizophrenia. (3) An influence of blood brain–barrier changes on levels of S100B in serum cannot be completely ruled out owing to a trend towards higher albumin CSF/serum quotients in the schizophrenia group (p
0.11, table 1). (4) A degenerative loss of immature oligodendrocytes that are MBP‐negative but S100B‐positive, or a loss of astrocytes which are GFAP‐negative but may be expressing S100B cannot be ruled out.3
In summary, our finding of increased levels of S100B in patients with schizophrenia without an indication for significant glial (GFAP, MBP) or neuronal (NSE) damage may be interpreted as indirect evidence for an increased active secretion of S100B in the brain during an acute psychotic episode in first‐onset schizophrenia.