Traumatic Brain Injury Elevates the Alzheimer's Amyloid Peptide Abeta42 in Human CSF: A Possible Role for Nerve Cell Injury

Autor: Charlotte Raby, Alex E. Roher, P. F. Stahel, Lori M. Evans, Katharyn Spiegel, Mark R. Emmerling, T. Kossmann, Yu Min Kuo, P. D. Mehta, M. C. Morganti-Kossmann, M. D. Watson
Rok vydání: 2000
Předmět:
Zdroj: Annals of the New York Academy of Sciences. 903:118-122
ISSN: 1749-6632
0077-8923
DOI: 10.1111/j.1749-6632.2000.tb06357.x
Popis: 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 tau, 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 CSF 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.
Databáze: OpenAIRE