ArticleClinical and experimental emergency medicine2025
The long-term influences of age at injury on neuroinflammation and neuronal apoptosis following traumatic brain injury in pediatric and adult mice.
Article in Clinical and experimental emergency medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Extracellular vesicles as biomarkers for traumatic brain injury using a 3D in vitro human brain tissue model.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
objectiveThe study explores the long-term impacts of traumatic brain injury (TBI) on neuroinflammation and neuronal apoptosis in pediatric and adult mice, focusing on how age at injury influences these processes.
methodsControlled cortical impacts were used to induce TBI in pediatric (21-25 days old) and adult (8-12 weeks old) C57BL/6 male mice. Neuroinflammation was evaluated by measuring immunoreactivity for allograft inflammatory factor 1 (AIF-1)/ionized calcium-binding adaptor molecule 1 (Iba-1) and glial fibrillary acidic protein (GFAP), while apoptosis was assessed using markers such as B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), Bcl-2, and procaspase-3. Additionally, heat shock protein 70 (HSP70) expression was measured to understand the stress response.
resultsFollowing controlled cortical impacts, pediatric mice exhibited a significant reduction in expression of neuronal nuclei (P<0.001), and significant increases in expression of GFAP (P<0.01) and AIF-1/Iba-1 (P<0.05) at 3 days post-injury (DPI) compared with sham controls. In contrast, adult mice exhibited no significant change in AIF-1/Iba-1 expression and a less pronounced increase in GFAP (P<0.05) at 3 DPI compared with sham controls. A more significant increase in Bax/Bcl-2 ratio at 7 DPI (P<0.01) was seen in pediatric mice, while a weak but significant increase in Bax/Bcl-2 ratio at 7 DPI (P<0.05) was evident in adults. Both age groups showed a significant but transient increase in HSP70 levels at 7 DPI, which normalized by 90 DPI.
conclusionPediatric and adult mice exhibited significant time-dependent differences in neuroinflammation and apoptosis following TBI, with pediatric mice showing more intense early responses indicative of age-specific vulnerabilities in post-injury outcomes. Both age groups showed a significant but transient increase in HSP70 expression, suggesting an acute response to stress post-injury.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.