The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
In Vitro Models of Traumatic Brain Injury
Abstract
In vitro models of traumatic brain injury (TBI) are helping elucidate the pathobiological mechanisms responsible for dysfunction and delayed cell death after mechanical stimulation of the brain. Researchers have identified compounds that have the potential to break the chain of molecular events set in motion by traumatic injury. Ultimately, the utility of in vitro models in identifying novel therapeutics will be determined by how closely the in vitro cascades recapitulate the sequence of cellular events that play out in vivo after TBI. Herein, the major in vitro models are reviewed, and a discussion of the physical injury mechanisms and culture preparations is employed. A comparison between the efficacy of compounds tested in vitro and in vivo is presented as a critical evaluation of the fidelity of in vitro models to the complex pathobiology that is TBI. We conclude that in vitro models were greater than 88% predictive of in vivo results.
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Cites
ATP mediates rapid microglial response to local brain injury in vivo
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Mitochondrial membrane permeabilization in cell death
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The impact of traumatic brain injuries: A global perspective
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Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways
Hardingham, G. E., Fukunaga, Y., & Bading, H. (2002) · Nature Neuroscience · doi:10.1038/nn835 · Cited by 1,686
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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 · cited 4×
“Reactions involving free iron also produce ROS (128).”
BackgroundInfluentialFas ligand/Fas system in the brain: regulator of immune and apoptotic responses
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Biomechanical Analysis of Experimental Diffuse Axonal Injury
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“, calcium uptake), KB-R7943, blocked posttraumatic calcium increase and reduced cell death after moderate and severe biaxial stretch of astrocytes (121).”
Background
Cited by
Blood–brain barrier dysfunction following traumatic brain injury
Alluri, H., Wiggins-Dohlvik, K., Davis, M. L., Huang, J. H., & Tharakan, B. (2015) · Metabolic Brain Disease · doi:10.1007/s11011-015-9651-7 · Cited by 149
Oerter, S., Förster, C., & Bohnert, M. (2019) · International Journal of Legal Medicine · doi:10.1007/s00414-018-1893-6 · Cited by 43
Chronic Effects of Mild Neurotrauma: Putting the Cart Before the Horse?
Castellani, R. J., Perry, G., & Iverson, G. L. (2015) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0000000000000193 · Cited by 40
Impact of traumatic brain injury on amyotrophic lateral sclerosis: from bedside to bench
Franz, C. K., Joshi, D., Daley, E. L., Grant, R. A., Dalamagkas, K., Leung, A., Finan, J. D., & Kiskinis, E. (2019) · Journal of Neurophysiology · doi:10.1152/jn.00572.2018 · Cited by 26
Rue, M. C. P., Alonso, L. M., & Marder, E. (2022) · iScience · doi:10.1016/j.isci.2022.104919 · Cited by 15
Metadata
- Authors
- Morrison, B., Elkin, B. S., Dollé, J.-P., & Yarmush, M. L.
- Venue
- Annual Review of Biomedical Engineering
- Publisher
- Annual Reviews
- Published
- 2011-08-15
- Volume
- 13
- Issue
- 1
- Pages
- 91-126
- ISSN
- 1523-9829 (ISSN-L)
- 1545-4274
- OpenAlex
- W2132907436
- Cited by
- 227
- References
- 13
- FWCI
- 1.27
- Type
- journal article
- Language
- en
- Open access
- closed
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- Morrison, B., Elkin, B. S., Dollé, J.-P., & Yarmush, M. L. (2011). In Vitro Models of Traumatic Brain Injury. Annual Review of Biomedical Engineering. https://doi.org/10.1146/annurev-bioeng-071910-124706
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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