Traumatic brain injury elevates the Alzheimer's amyloid peptide Aβ42 in human CSF -: A possible role for nerve cell injury

The increased risk for Alzheimer's Disease (AD) associated with traumatic brain injury (TBI) suggests that environmental insults may influence the development of this age-related dementia, Recently, we have shown that the levels of the beta-amyloid peptide (A beta(1-42)) increase in the cerebrospinal fluid (CSF) of patients after severe brain injury and remain elevated for some time after the initial event, The relationships of elevated A beta with markers of blood-brain barrier (BBB) disruption, inflammation, and nerve cell or axonal injury were evaluated in CSF samples taken daily from TBI patients, This analysis reveals that the rise in A beta(1-42) is best correlated with possible markers of neuronal or axonal injury, the cytoskeletal protein tan, neuron-specific enolase (NSE), and apolipoprotein E (ApoE), Similar or better correlations were observed between A beta(1-40) and the three aforementioned markers, These results imply that the degree of brain injury may play a decisive role in determining the levels of A beta(1-42) and A beta(1-40) in the CSP of TBI patients, inflammation and alterations in BBB may play lesser, but nonetheless significant, roles In determining the A beta level in CSF after brain injury.