The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Neuroinflammation and blood–brain barrier disruption following traumatic brain injury: Pathophysiology and potential therapeutic targets
Open accessAbstract
Traumatic Brain Injury (TBI) is the most frequent cause of death and disability in young adults and children in the developed world, occurring in over 1.7 million persons and resulting in 50,000 deaths in the United States alone. The Centers for Disease Control and Prevention estimate that between 3.2 and 5.3 million persons in the United States live with a TBI‐related disability, including several neurocognitive disorders and functional limitations. Following the primary mechanical injury in TBI, literature suggests the presence of a delayed secondary injury involving a variety of neuroinflammatory changes. In the hours to days following a TBI, several signaling molecules and metabolic derangements result in disruption of the blood–brain barrier, leading to an extravasation of immune cells and cerebral edema. The primary, sudden injury in TBI occurs as a direct result of impact and therefore cannot be treated, but the timeline and pathophysiology of the delayed, secondary injury allows for a window of possible therapeutic options. The goal of this review is to discuss the pathophysiology of the primary and delayed injury in TBI as well as present several preclinical studies that identify molecular targets in the potential treatment of TBI. Additionally, certain recent clinical trials are briefly discussed to demonstrate the current state of TBI investigation.
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Cites
Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo
Nimmerjahn, A., Kirchhoff, F., & Helmchen, F. (2005) · Science · doi:10.1126/science.1110647 · Cited by 5,827
Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17
Baker, M., Mackenzie, I. R., Pickering-Brown, S. M., Gass, J., Rademakers, R., Lindholm, C., Snowden, J., Adamson, J., Sadovnick, A. D., Rollinson, S., et al. (2006) · Nature · doi:10.1038/nature05016 · Cited by 2,058
Axonal pathology in traumatic brain injury
Johnson, V. E., Stewart, W., & Smith, D. H. (2013) · Experimental Neurology · doi:10.1016/j.expneurol.2012.01.013 · Cited by 1,273
A controlled cortical impact model of traumatic brain injury in the rat
Edward Dixon, C., Clifton, G. L., Lighthall, J. W., Yaghmai, A. A., & Hayes, R. L. (1991) · Journal of Neuroscience Methods · doi:10.1016/0165-0270(91)90104-8 · Cited by 1,141
Yang, Y., Estrada, E. Y., Thompson, J. F., Liu, W., & Rosenberg, G. A. (2007) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/sj.jcbfm.9600375 · Cited by 1,060
Functional plasticity of macrophages: reversible adaptation to changing microenvironments
Stout, R. D., & Suttles, J. (2004) · Journal of Leukocyte Biology · doi:10.1189/jlb.0504272 · Cited by 751
Progranulin is a mediator of the wound response
He, Z., Ong, C. H. P., Halper, J., & Bateman, A. (2003) · Nature Medicine · doi:10.1038/nm816 · Cited by 490
Expression profiles for macrophage alternative activation genes in AD and in mouse models of AD.
(2006) · Journal of Neuroinflammation · doi:10.1186/1742-2094-3-27 · Cited by 393
Antioxidant Therapies for Traumatic Brain Injury
Hall, E. D., Vaishnav, R. A., & Mustafa, A. G. (2010) · Neurotherapeutics · doi:10.1016/j.nurt.2009.10.021 · Cited by 390
Rosenberg, G. A., Cunningham, L. A., Wallace, J., Alexander, S., Estrada, E. Y., Grossetete, M., Razhagi, A., Miller, K., & Gearing, A. (2001) · Brain Research · doi:10.1016/s0006-8993(00)03294-7 · Cited by 388
Schreibelt, G., Kooij, G., Reijerkerk, A., van Doorn, R., Gringhuis, S. I., van der Pol, S., Weksler, B. B., Romero, I. A., Couraud, P., Piontek, J., et al. (2007) · The FASEB Journal · doi:10.1096/fj.07-8329com · Cited by 347
Prakash, R., & Carmichael, S. T. (2015) · Current Opinion in Neurology · doi:10.1097/wco.0000000000000248 · Cited by 296
Haber, M., Abdel Baki, S. G., Grin'kina, N. M., Irizarry, R., Ershova, A., Orsi, S., Grill, R. J., Dash, P., & Bergold, P. J. (2013) · Experimental Neurology · doi:10.1016/j.expneurol.2013.09.002 · Cited by 95
Zhao, H., Zhang, X., Dai, Z., Feng, Y., Li, Q., Zhang, J. H., Liu, X., Chen, Y., & Feng, H. (2016) · Scientific Reports · doi:10.1038/srep23286 · Cited by 84
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Bernstein, D. L., Zuluaga-Ramirez, V., Gajghate, S., Reichenbach, N. L., Polyak, B., Persidsky, Y., & Rom, S. (2020) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x19882264 · Cited by 120
Jeon, M.-T., Kim, K.-S., Kim, E. S., Lee, S., Kim, J., Hoe, H.-S., & Kim, D.-G. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101333 · Cited by 76
Vargas-Rodríguez, P., Cuenca-Martagón, A., Castillo-González, J., Serrano-Martínez, I., Luque, R. M., Delgado, M., & González-Rey, E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241814117 · Cited by 25
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Metadata
- Authors
- Sulhan, S., Lyon, K. A., Shapiro, L. A., & Huang, J. H.
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2018-09-27
- Volume
- 98
- Issue
- 1
- Pages
- 19-28
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- OpenAlex
- W2893346879
- Cited by
- 317
- References
- 14
- FWCI
- 7.11
- Type
- journal article
- Language
- en
- Open access
- green
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