Citation

Bagnato S, Andriolo M, Boccagni C, Galardi G. Neuroreport 2017; 28(5): 250-252.

Affiliation

aRehabilitation Department, Unit of Neurophysiology and Unit for Severe Acquired Brain Injuries bClinical Pathology and Microbiology Laboratory, Giuseppe Giglio Foundation, Cefalù, Italy.

Copyright

(Copyright © 2017, Lippincott Williams and Wilkins)

DOI

10.1097/WNR.0000000000000748

PMID

28178070

Abstract

Traumatic brain injury (TBI) is a major risk factor for Alzheimer's disease. Recent studies suggest that amyloid-beta (Aβ) deposit can be detected several years after TBI. However, it is unknown whether post-TBI Aβ deposits arise from short-term changes in Aβ metabolism or reflect a long-term sequela. To answer this question, we evaluated the cerebrospinal levels of Aβ several months after a severe TBI. The participants of this study were eight consecutive patients who developed a disorder of consciousness after a TBI, including seven in a minimally conscious state and one with unresponsive wakefulness syndrome (mean age: 35.4±14.2 years, mean time since brain injury 297.9±189.8 days). Cerebrospinal Aβ1-42 peptide was measured using a commercially available Aβ enzyme-linked immunoassay kit. Reduced Aβ1-42 levels were observed in seven of eight (87.5%) patients with severe post-TBI disorders of consciousness, with the magnitude of reduction among these seven patients ranging from 27 to 75.1% of the lower normal limit. These results point to prolonged changes in Aβ metabolism after a TBI and they suggest a potential mechanism of long-term neurotoxicity.

Language: en