Traumatic Brain Injury Elevates the Alzheimer's Amyloid Peptide Aβ42 in Human CSF: A Possible Role for Nerve Cell Injury

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Abstract
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 β-amyloid peptide (Aβ1–42) 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 Aβ 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 Aβ1–42 is best correlated with possible markers of neuronal or axonal injury, the cytoskeletal protein tau, neuron-specific enolase (NSE), and apolipoprotein E (ApoE). Similar or better correlations were observed between Aβ1–40 and the three aforementioned markers. These results imply that the degree of brain injury may play a decisive role in determining the levels of Aβ1–42 and Aβ1–40 in the CSF of TBI patients. Inflammation and alterations in BBB may play lesser, but nonetheless significant, roles in determining the Aβ level in CSF after brain injury.