The DOI matches its Crossref record; 105 of the 105 references it cites were found in a registry or an index.
Microglia Activation as a Biomarker for Traumatic Brain Injury
Open accessAbstract
Traumatic brain injury (TBI) has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inflammatory responses accompany TBI. A series of inflammatory cytokines and chemokines spreads to normal brain areas juxtaposed to the core impacted tissue. Among the repertoire of immune cells involved, microglia is a key player in propagating inflammation to tissues neighboring the core site of injury. Neuroprotective drug trials in TBI have failed, likely due to their sole focus on abrogating neuronal cell death and ignoring the microglia response despite these inflammatory cells' detrimental effects on the brain. Another relevant point to consider is the veracity of results of animal experiments due to deficiencies in experimental design, such as incomplete or inadequate method description, data misinterpretation, and reporting may introduce bias and give false-positive results. Thus, scientific publications should follow strict guidelines that include randomization, blinding, sample-size estimation, and accurate handling of all data (Landis et al., 2012). A prolonged state of inflammation after brain injury may linger for years and predispose patients to develop other neurological disorders, such as Alzheimer's disease. TBI patients display progressive and long-lasting impairments in their physical, cognitive, behavioral, and social performance. Here, we discuss inflammatory mechanisms that accompany TBI in an effort to increase our understanding of the dynamic pathological condition as the disease evolves over time and begin to translate these findings for defining new and existing inflammation-based biomarkers and treatments for TBI.
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Citations
Cites
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Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner
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The many faces of macrophage activation
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“…(b) stimulate microglia to polarize into the M2 phenotype, (c) promote synaptic, neuronal plasticity, and cell survival at a close or distal range from the area of injury, and (d) reduce the inflammatory response post-TBI (Mosser, 2003; Gordon and Taylor, 2005; Ben Achour and Pascual, 2010).”
BackgroundInfluentialMicroglia as a source and target of cytokines
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“Likewise, endogenous inducers act as inflammatory mediators, such as platelet-activating factor (PAF), lipids, serum proteins, or complement factors; additionally, disturbances in ATP and [K+] levels may cause microglia activation (Hanisch, 2002).”
BackgroundControl of microglial neurotoxicity by the fractalkine receptor
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Inflammation after trauma: Microglial activation and traumatic brain injury
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Cited by
Neuroimmunology of Traumatic Brain Injury: Time for a Paradigm Shift
Jassam, Y. N., Izzy, S., Whalen, M., McGavern, D. B., & El Khoury, J. (2017) · Neuron · doi:10.1016/j.neuron.2017.07.010 · Cited by 799
Inflammatory Response in the CNS: Friend or Foe?
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Call off the dog(ma): M1/M2 polarization is concurrent following traumatic brain injury
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Li, R.-Y., Qin, Q., Yang, H.-C., Wang, Y.-Y., Mi, Y.-X., Yin, Y.-S., Wang, M., Yu, C.-J., & Tang, Y. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00542-y · Cited by 204
Time-dependent effects of CX3CR1 in a mouse model of mild traumatic brain injury
Febinger, H. Y., Thomasy, H. E., Pavlova, M. N., Ringgold, K. M., Barf, P. R., George, A. M., Grillo, J. N., Bachstetter, A. D., Garcia, J. A., Cardona, A. E., et al. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0386-5 · Cited by 110
“A consensus based on recent evidence considers neuroinflammation as an important secondary mechanism that plays a role in delaying injury after TBI [1 – 3].”
Metadata
- Authors
- Hernandez-Ontiveros, D. G., Tajiri, N., Acosta, S., Giunta, B., Tan, J., & Borlongan, C. V.
- Venue
- Frontiers in Neurology
- Publisher
- Frontiers Media SA
- Published
- 2013
- Volume
- 4
- Pages
- 30-30
- ISSN
- 1664-2295 (ISSN-L)
- OpenAlex
- W1966308623
- Cited by
- 277
- References
- 105
- FWCI
- 15.77
- Type
- journal article
- Language
- en
- Open access
- gold
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- Hernandez-Ontiveros, D. G., Tajiri, N., Acosta, S., Giunta, B., Tan, J., & Borlongan, C. V. (2013). Microglia Activation as a Biomarker for Traumatic Brain Injury. Frontiers in Neurology. https://doi.org/10.3389/fneur.2013.00030
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
