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Cellular players that shape evolving pathology and neurodegeneration following traumatic brain injury
Puntambekar SS, Saber M, Lamb BT, Kokiko-Cochran ON.. Brain, behavior, and immunity, 2018-03-27
Topic: Brain proteins, microglia and lab models
Traumatic brain injury (TBI) is one of the leading causes of death and disability worldwide, and has emerged as a critical risk factor for multiple neurodegenerative diseases, particularly Alzheimer's disease (AD). How the inflammatory cascade resulting from mechanical stress, axonal shearing and the loss of neurons and glia following initial impact in TBI, contributes to the development of AD-like disease is unclear. Neuroinflammation, characterized by blood-brain barrier (BBB) dysfunction and activation of brain-resident microglia and astrocytes, resulting in secretion of inflammatory mediators and subsequent recruitment of peripheral immune cells has been the focus of extensive research in attempts to identify drug-targets towards improving functional outcomes post TBI.
Key findings
- How the inflammatory cascade resulting from mechanical stress, axonal shearing and the loss of neurons and glia following initial impact in TBI, contributes to the development of AD-like disease is unclear.
- Neuroinflammation, characterized by blood-brain barrier (BBB) dysfunction and activation of brain-resident microglia and astrocytes, resulting in secretion of inflammatory mediators and subsequent recruitment of peripheral immune cells has been the focus of extensive research in attempts to identify drug-targets towards improving functional outcomes post TBI.
- While knowledge of intricate cellular interactions that shape lesion pathophysiology is incomplete, a major limitation in the field is the lack of understanding of how distinct cell types differentially alter TBI pathology.
- The aim of this review is to highlight functional differences between populations of bone marrow derived, infiltrating monocytes/macrophages and brain-resident microglia based on differential expression of the chemokine receptors CCR2 and CX 3 CR1.
Why it matters
This review discusses how neuroinflammation after traumatic brain injury may contribute to Alzheimer's-like disease and notes that drug targets are being sought. It does not test a treatment or cure.
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Study details
- Evidence strengthLow
How this study scored 39/100
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, behavior, and immunity) |
| Journal's citation record | 2 / 4 | Brain Behavior and Immunity: journal h-index 249 (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 | 2 / 5 | 2018 — within 10 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 | 4 / 7 | Cited 77 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.7 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 3 / 6 | Cited 5.8× 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 | 2 / 4 | Cited 24 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Olga N. Kokiko‐Cochran: h-index 26 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | The Ohio State University: institution h-index 1,378 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29601944) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 39 / 100 | — |
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Read the original
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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
Puntambekar, S. S., Saber, M., Lamb, B. T., & Kokiko-Cochran, O. N. (2018). Cellular players that shape evolving pathology and neurodegeneration following traumatic brain injury. Brain, behavior, and immunity. https://doi.org/10.1016/j.bbi.2018.03.033
Vancouver
Puntambekar SS, Saber M, Lamb BT, Kokiko-Cochran ON. Cellular players that shape evolving pathology and neurodegeneration following traumatic brain injury. Brain, behavior, and immunity. 2018. doi:10.1016/j.bbi.2018.03.033. PMID: 29601944.
BibTeX
@article{puntambekar2018-29601944,
author = {Puntambekar, S. S. and Saber, M. and Lamb, B. T. and Kokiko-Cochran, O. N.},
title = {{Cellular players that shape evolving pathology and neurodegeneration following traumatic brain injury}},
journal = {Brain, behavior, and immunity},
year = {2018},
doi = {10.1016/j.bbi.2018.03.033},
pmid = {29601944},
url = {https://doi.org/10.1016/j.bbi.2018.03.033}
}
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