The DOI matches its Crossref record; 104 of the 104 references it cites were found in a registry or an index.
Cell Death Mechanisms and Modulation in Traumatic Brain Injury
Open accessAbstract
SummaryCell death after traumatic brain injury (TBI) is a major cause of neurological deficits and mortality. Understanding the mechanisms of delayed post-traumatic cell loss may lead to new therapies that improve outcome. Although TBI induces changes in multiple cell types, mechanisms of neuronal cell death have been the predominant focus. Recent work has emphasized the diversity of neuronal death phenotypes, which have generally been defined by either morphological or molecular changes. This diversity has led to confusing and at times contradictory nomenclature. Here we review the historical basis of proposed definitions of neuronal cell death, with the goal of clarifying critical research questions and implications for therapy in TBI. We believe that both morphological and molecular features must be used to clarify post-traumatic cell death and related therapeutic targets. Further, we underscore that the most effective neuroprotective strategies will need to target multiple pathways to reflect the regional and temporal changes underlying diverse neuronal cell death phenotypes.
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Traumatic Brain Injuries: Pathophysiology and Potential Therapeutic Targets
Ng, S. Y., & Lee, A. Y. W. (2019) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2019.00528 · Cited by 852
Microglia/Macrophage Polarization Dynamics in White Matter after Traumatic Brain Injury
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Traumatic brain injury: A risk factor for Alzheimer's disease
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Metadata
- Authors
- Stoica, B. A., & Faden, A. I.
- Venue
- Neurotherapeutics
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 7
- Issue
- 1
- Pages
- 3-12
- ISSN
- 1878-7479 (ISSN-L)
- OpenAlex
- W2046802002
- Cited by
- 276
- References
- 104
- FWCI
- 10.42
- Type
- journal article
- Language
- en
- Open access
- bronze
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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).
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