This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Dr. Peltz et al. examined whether blood-based biomarkers can differentiate older veterans with and without traumatic brain injury (TBI) and cognitive impairment in a cross-sectional study of 155 veterans from 2 veterans' retirement homes. They found that increased levels of blood-based, CNS-enriched exosomal biomarkers—particularly phosphorylated tau (p-tau), neurofilament light (NfL), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α)—were associated with cognitive impairment and TBI. In response, Drs. Wisniewski and Fossati question the clinical utility of these biomarkers, suggesting that the differences in these biomarkers may be driven more by the presence of cognitive impairment rather than the history of TBI. They argue that there is no proven causal relationship between the remote TBI and the observed cognitive impairment in this group and point to the absence of differences in any of the biomarkers in the control group and the TBI group without cognitive impairment to support their position. They also note a previous article from the group in which amyloid beta 42 (Aβ42) was reported to be elevated for decades after TBI, not replicated in this article. Responding to these comments, the authors agree that their findings are most likely explained by cognitive impairment but argue that the biomarkers could differentiate non–TBI-related cognitive impairment from TBI-associated cognitive impairment. They acknowledge the differences in results between their 2 biomarker articles but note that different assays were used, analyzed in different laboratories, and that the samples were overlapping but different. Nevertheless, they hypothesize that biomarkers for TBI-associated cognitive impairment are likely to differ from classic biomarkers for Alzheimer disease. This exchange highlights the challenges of disentangling the cognitive effects of remote TBI from other causes of cognitive impairment and the potential variability in the results of biomarker studies depending on the assays and laboratories used.
Dr. Peltz et al. examined whether blood-based biomarkers can differentiate older veterans with and without traumatic brain injury (TBI) and cognitive impairment in a cross-sectional study of 155 veterans from 2 veterans' retirement homes. They found that increased levels of blood-based, CNS-enriched exosomal biomarkers—particularly phosphorylated tau (p-tau), neurofilament light (NfL), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α)—were associated with cognitive impairment and TBI. In response, Drs. Wisniewski and Fossati question the clinical utility of these biomarkers, suggesting that the differences in these biomarkers may be driven more by the presence of cognitive impairment rather than the history of TBI. They argue that there is no proven causal relationship between the remote TBI and the observed cognitive impairment in this group and point to the absence of differences in any of the biomarkers in the control group and the TBI group without cognitive impairment to support their position. They also note a previous article from the group in which amyloid beta 42 (Aβ42) was reported to be elevated for decades after TBI, not replicated in this article. Responding to these comments, the authors agree that their findings are most likely explained by cognitive impairment but argue that the biomarkers could differentiate non–TBI-related cognitive impairment from TBI-associated cognitive impairment. They acknowledge the differences in results between their 2 biomarker articles but note that different assays were used, analyzed in different laboratories, and that the samples were overlapping but different. Nevertheless, they hypothesize that biomarkers for TBI-associated cognitive impairment are likely to differ from classic biomarkers for Alzheimer disease. This exchange highlights the challenges of disentangling the cognitive effects of remote TBI from other causes of cognitive impairment and the potential variability in the results of biomarker studies depending on the assays and laboratories used.
Footnotes
Author disclosures are available upon request (journal{at}neurology.org).
- © 2021 American Academy of Neurology
AAN Members
We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page.
AAN Non-Member Subscribers
Purchase access
Letters: Rapid online correspondence
REQUIREMENTS
You must ensure that your Disclosures have been updated within the previous six months. Please go to our Submission Site to add or update your Disclosure information.
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
