Background: Traumatic brain injury (TBI) is a major risk factor for Alzheimer's disease (AD). Although the mechanisms that lead to AD after a TBI are unclear, we hypothesize that changes in amyloid-β (Aβ) metabolism and abnormal tau phosphorylation are reasonable candidates.
Objective: To investigate Aβ and tau dynamics in the chronic phase of TBI.
Methods: We evaluated Aβ1-42, total tau (t-tau), and phosphorylated tau (p-tau) levels in the cerebrospinal fluid (CSF) of 15 patients who developed a prolonged disorder of consciousness after a severe TBI (mean time from TBI 271.6 ± 176.5 days).
Results: Reduced Aβ1-42 levels (median 258 pg/ml, range 90-833.6) were observed in 14/15 patients (93.3%) with severe post-TBI disorders of consciousness. These CSF analysis data did not correlate with time since TBI or with the patients' level of consciousness as determined by the Coma Recovery Scale Revised. Normal t-tau levels (median 95.2 pg/ml, range 52-256.9) were found in all patients. Normal p-tau levels (median 22.2 pg/ml, range 14-72) were observed in 14/15 patients, with just a single patient having a slightly increased p-tau level.
Conclusion: The present findings show that Aβ and tau are differently affected in the chronic phase of severe TBI.
Keywords: Amyloid beta; phosphorylated tau; total tau; traumatic brain injury; vegetative state.