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Traumatic Brain Injury and Chronic Traumatic Encephalopathy: Not Only Trigger for Neurodegeneration but Also for Cerebral Amyloid Angiopathy?
Marialuisa Zedde, Fabrizio Piazza, Rosario Pascarella. Biomedicines, 2025-04-05
Topic: Brain proteins, microglia and lab models
Traumatic brain injury (TBI) has been linked to the development of neurodegenerative diseases, particularly Alzheimer's disease (AD) and chronic traumatic encephalopathy (CTE). This review critically assesses the relationship between TBI and cerebral amyloid angiopathy (CAA), highlighting the complexities of diagnosing CAA in the context of prior head trauma. While TBI has been shown to facilitate the accumulation of amyloid plaques and tau pathology, the interplay between neurodegenerative processes and vascular contributions remains underexplored. Epidemiological studies indicate that TBI increases the risk of various dementias, not solely AD, emphasizing the need for a comprehensive understanding of TBI-related neurodegeneration as a polypathological condition. This review further delineates the mechanisms by which TBI can lead to CAA, particularly focusing on the vascular changes that occur post-injury. It discusses the challenges associated with diagnosing CAA after TBI, particularly due to the overlapping symptoms and pathologies that complicate clinical evaluations. Notably, this review includes a clinical case that exemplifies the diagnostic challenges posed by TBI in patients with subsequent cognitive decline and vascular pathology. By synthesizing current research on TBI, CAA, and associated neurodegenerative conditions, this review aims to foster a more nuanced understanding of how these conditions interact and contribute to long-term cognitive outcomes. The findings underscore the importance of developing standardized diagnostic criteria and imaging techniques to better elucidate the relationship between TBI and vascular pathology, which could enhance clinical interventions and inform therapeutic strategies for affected individuals.
Key findings
- Epidemiological studies indicate that TBI increases the risk of various dementias, not solely AD, emphasizing the need for a comprehensive understanding of TBI-related neurodegeneration as a polypathological condition.
- It discusses the challenges associated with diagnosing CAA after TBI, particularly due to the overlapping symptoms and pathologies that complicate clinical evaluations.
Why it matters
This review examines the possible relationship between traumatic brain injury and cerebral amyloid angiopathy, noting that diagnosing CAA after head trauma is difficult because symptoms and pathologies overlap. It raises questions for future research rather than reporting any treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 40/100
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 (Biomedicines) |
| Journal's citation record | 1 / 4 | Biomedicines: journal h-index 133 (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 | 4 / 5 | 2025 — within 3 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 | 2 / 7 | Cited 12 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 6.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 12 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Rosario Pascarella: h-index 25 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Milano-Bicocca: institution h-index 723 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40299513) |
| Free to read | 2 / 2 | Free to read |
| Total | 40 / 100 | — |
What each of these 20 components measures, and what this score is not →
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
Zedde, M., Piazza, F., & Pascarella, R. (2025). Traumatic Brain Injury and Chronic Traumatic Encephalopathy: Not Only Trigger for Neurodegeneration but Also for Cerebral Amyloid Angiopathy? Biomedicines. https://doi.org/10.3390/biomedicines13040881
Vancouver
Zedde M, Piazza F, Pascarella R. Traumatic Brain Injury and Chronic Traumatic Encephalopathy: Not Only Trigger for Neurodegeneration but Also for Cerebral Amyloid Angiopathy? Biomedicines. 2025. doi:10.3390/biomedicines13040881. PMID: 40299513.
BibTeX
@article{zedde2025-40299513,
author = {Zedde, Marialuisa and Piazza, Fabrizio and Pascarella, Rosario},
title = {{Traumatic Brain Injury and Chronic Traumatic Encephalopathy: Not Only Trigger for Neurodegeneration but Also for Cerebral Amyloid Angiopathy?}},
journal = {Biomedicines},
year = {2025},
doi = {10.3390/biomedicines13040881},
pmid = {40299513},
url = {https://doi.org/10.3390/biomedicines13040881}
}
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