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49/100

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Risk factors

Topic: Brain proteins, microglia and lab models

Traumatic brain injury (TBI) is a risk factor for dementia. Mixed neurodegenerative pathologies have been described in late survivors of TBI, but the mechanisms driving post-TBI neurodegeneration remain elusive. Increasingly, blood-brain barrier (BBB) disruption has been recognized in a range of neurologic disorders including dementias, but little is known of the consequences of TBI on the BBB. Autopsy cases of single moderate or severe TBI from the Glasgow TBI Archive (n = 70) were selected to include a range from acute (10 hours-13 days) to long-term (1-47 years) survival, together with age-matched uninjured controls (n = 21). Multiple brain regions were examined using immunohistochemistry for the BBB integrity markers fibrinogen and immunoglobulin G. After TBI, 40% of patients dying in the acute phase and 47% of those surviving a year or more from injury showed multifocal, abnormal, perivascular, and parenchymal fibrinogen and immunoglobulin G immunostaining localized to the gray matter, with preferential distribution toward the crests of gyri and deep neocortical layers. In contrast, when present, controls showed only limited localized immunostaining. These preliminary data demonstrate evidence of widespread BBB disruption in a proportion of TBI patients emerging in the acute phase and, intriguingly, persisting in a high proportion of late survivors.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Hay, JR., Johnson, V. E., Young, A. M., Smith, D. H., & Stewart, W. (2015). Blood-Brain Barrier Disruption Is an Early Event That May Persist for Many Years After Traumatic Brain Injury in Humans. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/nen.0000000000000261

Vancouver

Hay JR, Johnson VE, Young AM, Smith DH, Stewart W. Blood-Brain Barrier Disruption Is an Early Event That May Persist for Many Years After Traumatic Brain Injury in Humans. Journal of neuropathology and experimental neurology. 2015. doi:10.1097/nen.0000000000000261. PMID: 26574669.

BibTeX

@article{hay2015-26574669,
  author  = {Hay, JR. and Johnson, V. E. and Young, A. M. and Smith, D. H. and Stewart, W.},
  title   = {{Blood-Brain Barrier Disruption Is an Early Event That May Persist for Many Years After Traumatic Brain Injury in Humans}},
  journal = {Journal of neuropathology and experimental neurology},
  year    = {2015},
  doi     = {10.1097/nen.0000000000000261},
  pmid    = {26574669},
  url     = {https://doi.org/10.1097/nen.0000000000000261}
}

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Key findings

Autopsy cases of single moderate or severe TBI from the Glasgow TBI Archive (n = 70) were selected to include a range from acute (10 hours-13 days) to long-term (1-47 years) survival, together with age-matched uninjured controls (n = 21).
Multiple brain regions were examined using immunohistochemistry for the BBB integrity markers fibrinogen and immunoglobulin G.
After TBI, 40% of patients dying in the acute phase and 47% of those surviving a year or more from injury showed multifocal, abnormal, perivascular, and parenchymal fibrinogen and immunoglobulin G immunostaining localized to the gray matter, with preferential distribution toward the crests of gyri and deep neocortical layers.
In contrast, when present, controls showed only limited localized immunostaining.
These preliminary data demonstrate evidence of widespread BBB disruption in a proportion of TBI patients emerging in the acute phase and, intriguingly, persisting in a high proportion of late survivors.

Why it matters

In brains from 70 people who died after a single moderate or severe head injury, 40% of those who died within days and 47% of those who lived a year or more (up to 47 years) showed blood proteins leaking into brain tissue, a sign that the blood-brain barrier was damaged; 21 uninjured controls showed only limited staining. The authors call these data "preliminary": the study suggests barrier damage may start early and last for years after injury, but it did not measure dementia, did not study mild injuries or living patients, and tested no treatment.

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Study details

Participants70
Evidence strengthLow

How this study scored 49/100

Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology)
Journal's citation record	2 / 4	Journal of Neuropathology & Experimental Neurology: journal h-index 239 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2015 — within 20 year(s) of the newest study here
Sample size	1 / 4	70 participants
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	3 / 3	Studied in people (participant count stated)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 245 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	18.8 citations a year over 13 year(s) since 2015
Impact for its field and year	3 / 6	Cited 7.4× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 6 other studies in this library
Still being cited	3 / 4	Cited 59 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author William B. Stewart Jr.: h-index 72 (OpenAlex, whole career)
Institution's track record	2 / 3	University of Pennsylvania: institution h-index 1,859 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 3 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 26574669)
Free to read	0 / 2	Behind a paywall — scores zero
Total	49 / 100	—

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