Research Reports - Monitoring of β-amyloid dynamics after traumatic brain injury

J Neurotrauma. 2013 Jul 7

Marklund N, Farrokhnia N, Hånell A, Vanmechelen E, Enblad P, Zetterberg H, Blennow K, Hillered L

Epidemiological evidence links severe or repeated traumatic brain injury (TBI) to
the development of Alzheimer's disease (AD). Accumulation of amyloid precursor
protein (APP) occurs with high frequency after TBI, particularly in injured
axons, and APP may be cleaved to amyloid-β (Aβ) peptides playing key
pathophysiological roles in AD. We used cerebral microdialysis (MD) to test the
hypothesis that interstitial Aβ levels are altered following TBI and related to
the injury type, cerebral energy metabolism, age of the patient and the level of
consciousness. In the present report, we evaluated 10 mechanically ventilated
patients (7 male, 3 female, age 18-76 years) with a severe TBI who had
intracranial pressure and MD monitoring. Each MD sample was analyzed for hourly
routine energy metabolic biomarkers (MD-lactate, MD-pyruvate, MD-glucose and
MD-lactate/pyruvate ratio), cellular distress biomarkers (MD-glutamate,
MD-glycerol) and MD-urea. The remaining MD samples were analyzed for Aβ1-40
(Aβ40; n= 765 samples) and Aβ1-42 (Aβ42; n= 765 samples) in pooled 2-hour
fractions up to 14 days post-injury using the Luminex xMAP technique allowing
detection with high temporal resolution of the key Aβ peptides Aβ40 and Aβ42.
Data are presented using medians and 25th and 75th percentiles. Both Aβ40 and
Aβ42 were consistently higher in patients with predominately diffuse axonal
injury compared to patients with focal TBI at day 1- 6 post- injury, Aβ42 being
significantly increased at 113-116 hours post-injury (p<0.05). The Aβ levels did
not correlate with the interstitial energy metabolic situation, age of the
patient or the level of consciousness. These results support that interstitial
generation of potentially toxic Aβ species may occur following human TBI,
particularly related to axonal injury.

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