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The neuropathology of chronic traumatic encephalopathy
McKee AC, Stein TD, Kiernan PT, Alvarez VE.. Brain pathology (Zurich, Switzerland), 2015-05-01
Topic: Brain proteins, microglia and lab models
Repetitive brain trauma is associated with a progressive neurological deterioration, now termed as chronic traumatic encephalopathy (CTE). Most instances of CTE occur in association with the play of sports, but CTE has also been reported in association with blast injuries and other neurotrauma. Symptoms of CTE include behavioral and mood changes, memory loss, cognitive impairment and dementia. Like many other neurodegenerative diseases, CTE is diagnosed with certainty only by neuropathological examination of brain tissue. CTE is a tauopathy characterized by the deposition of hyperphosphorylated tau (p-tau) protein as neurofibrillary tangles, astrocytic tangles and neurites in striking clusters around small blood vessels of the cortex, typically at the sulcal depths. Severely affected cases show p-tau pathology throughout the brain. Abnormalities in phosphorylated 43 kDa TAR DNA-binding protein are found in most cases of CTE; beta-amyloid is identified in 43%, associated with age. Given the importance of sports participation and physical exercise to physical and psychological health as well as disease resilience, it is critical to identify the genetic risk factors for CTE as well as to understand how other variables, such as stress, age at exposure, gender, substance abuse and other exposures, contribute to the development of CTE.
Key findings
- Repetitive brain trauma is associated with a progressive neurological deterioration, now termed as chronic traumatic encephalopathy (CTE).
- Abnormalities in phosphorylated 43 kDa TAR DNA-binding protein are found in most cases of CTE; beta-amyloid is identified in 43%, associated with age.
Why it matters
This review describes chronic traumatic encephalopathy as a tauopathy linked to repetitive brain trauma, with symptoms that can include memory loss, cognitive impairment and dementia, and notes it can only be diagnosed with certainty by neuropathological examination. It states that identifying genetic risk factors and understanding how other variables contribute to its development is critical.
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Study details
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Brain pathology (Zurich, Switzerland)) |
| Journal's citation record | 2 / 4 | Brain Pathology: journal h-index 183 (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 | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 584 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 44.9 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 5 / 6 | Cited 34.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 17 other studies in this library |
| Still being cited | 3 / 4 | Cited 156 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Victor E. Alvarez: h-index 45 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Boston University: institution h-index 1,456 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 25904048) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 48 / 100 | — |
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Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
McKee, A. C., Stein, T. D., Kiernan, P. T., & Alvarez, V. E. (2015). The neuropathology of chronic traumatic encephalopathy. Brain pathology (Zurich, Switzerland). https://doi.org/10.1111/bpa.12248
Vancouver
McKee AC, Stein TD, Kiernan PT, Alvarez VE. The neuropathology of chronic traumatic encephalopathy. Brain pathology (Zurich, Switzerland). 2015. doi:10.1111/bpa.12248. PMID: 25904048.
BibTeX
@article{mckee2015-25904048,
author = {McKee, A. C. and Stein, T. D. and Kiernan, P. T. and Alvarez, V. E.},
title = {{The neuropathology of chronic traumatic encephalopathy}},
journal = {Brain pathology (Zurich, Switzerland)},
year = {2015},
doi = {10.1111/bpa.12248},
pmid = {25904048},
url = {https://doi.org/10.1111/bpa.12248}
}
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