Abstract
The article by Peltz et al.1 provides a nice example of differences in neurodegenerative biomarkers which can be found in patients with chronic traumatic brain injury (TBI) using blood samples enriched for CNS-derived exosomes. However, these differences seem driven more by the presence of cognitive impairment (CI) rather than the history of TBI itself. Based on the cohort studied (older veterans), there is no proven causality demonstrating that the CI in the TBI-CI group is actually driven by the remote TBI, which occurred decades previously. This could be an independent clinical finding in the veterans. Because the control group and the TBI-no-CI group did not differ in any of the biomarkers, it seems that the main driver of differences is cognitive impairment, which could be independent from the TBI even in the TBI-CI group. This article has some overlap with a recent study from this group, in which Aβ42 was reported to be elevated for decades after TBI.2 This is not the case in this article, with no clear explanation. One wonders the utility of these biomarkers in a clinical setting because they do not clarify the causes of the CI and are not specific to TBI.
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