Inflammation and white matter degeneration persist for years after a single traumatic brain injury.
By Victoria E. Johnson, J. Stewart, F. Begbie, John Q. Trojanowski, Douglas H. Smith, W. Stewart. Brain : a journal of neurology, 2013
980 citations recorded by the source corpus.
Subfields: Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/ebd040da32dec026ae33769afb7734703c45271e
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Citations in the corpus
- Coupled Proliferation and Apoptosis Maintain the Rapid Turnover of Microglia in the Adult Brain (2017, background): “…(blue), CD45low (green), or CD45high (yellow) Vav- eports 18, 391–405, January 10, 2017 401 (Bilbo and Schwarz, 2009), delayed inflammation after traumatic brain injury (TBI) (Johnson et al., 2013), or the onset of agerelated amyloid deposition after gestational inflammation (Krstic et al., 2012).”
- Microglia in the TBI Brain: The Good, The Bad, And The Dysregulated (2015, methodology): “Contents lists available at ScienceDirect Experimental Neurology j ourna l homepage: www.e lsev ie r .com/ locate /yexnr (TBI) (Faden and Loane, 2015; Johnson et al., 2013; Smith et al., 2013, 2012).”
- Traumatic Brain Injuries: Pathophysiology and Potential Therapeutic Targets (2019, background): “Progressive phagocytosis and persistent inflammatory responses are evident by the accumulation of macrophages and activated microglia in TBI survivors years after injury (Gentleman et al., 2004; Johnson et al., 2013).”