Increased cerebrospinal fluid cleaved tau protein (C-tau) levels suggest axonal damage in pediatric patients with brain tumors.

OBJECTIVE: This study aims to determine if cerebrospinal fluid/serum cleaved tau protein and CSF 9-hydroxyoctadecadienoic acid levels, reflecting potential biomarkers of overall neuronal injury and lipid peroxidation, respectively, are elevated in brain tumor patients compared with controls.
DESIGN: This article is a prospective clinical observational study.
SETTING: This study is conducted at a tertiary-care children's hospital. PATIENTS: Our participants are children younger than or equal to 18 years of age undergoing brain tumor surgery.
MEASUREMENTS AND MAIN RESULTS: During the study period, 26 consecutive patients newly diagnosed with brain tumors who met the inclusion criteria were prospectively enrolled. Baseline cerebrospinal fluid analysis of cleaved tau and 9-hydroxyoctadecadienoic acid were measured in 15 patients. Cerebrospinal fluid cleaved tau and 9-hydroxyoctadecadienoic acid levels were measured in 22 patients for post-surgery days 1 and 3. Serum cleaved tau levels were measured for 20 and 18 patients for post-surgery days 1 and 3, respectively. The presence of a brain tumor significantly increased the baseline cerebrospinal fluid cleaved tau levels but did not affect cerebrospinal fluid 9-hydroxyoctadecadienoic acid levels. Similarly, there was a significant increase in post-surgery day 1 cerebrospinal fluid cleaved tau levels from baseline (p = 0.01) and a trend toward significant decrease in post-surgery day 3 cerebrospinal fluid cleaved tau from day 1 (p = 0.07). 9-Hydroxyoctadecadienoic acid concentrations remained relatively constant over time with no differences noted between the control and brain tumor patients. There was a trend towards a significant association between cerebrospinal fluid cleaved tau levels and duration of symptoms (p = 0.07).
CONCLUSIONS: Cerebrospinal fluid cleaved tau levels in children with newly diagnosed brain tumors exhibit markedly elevated cerebrospinal fluid cleaved tau levels, suggesting axonal damage. This axonal injury does not seem to correlate with lipid peroxidation at least when as assessed by cerebrospinal fluid 9-hydroxyoctadecadienoic acid levels. There was no association found between the biomarkers and multiple independent variables obtained at pre- and post-tumor resection.