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Citation |
Flygt J, Gumucio A, Ingelsson M, Skoglund K, Holm J, Alafuzoff I, Marklund N. J. Neuropathol. Exp. Neurol. 2016; 75(6): 503-515. |
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Affiliation |
From the Department of Neuroscience, Neurosurgery (JF, KS, JH, NM), and Department of Public Health and Caring Sciences, Geriatrics (AG, MI), and Department of Immunology, Genetics and Pathology (IA), Uppsala University, Uppsala, Sweden. Niklas.Marklund@neuro.uu.se. |
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Copyright |
(Copyright © 2016, American Association of Neuropathologists, Publisher Lippincott Williams and Wilkins) |
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DOI |
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PMID |
27105664 |
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Abstract |
Oligodendrocyte (OL) death may contribute to white matter pathology, a common cause of network dysfunction and persistent cognitive problems in patients with traumatic brain injury (TBI). Oligodendrocyte progenitor cells (OPCs) persist throughout the adult CNS and may replace dead OLs. OL death and OPCs were analyzed by immunohistochemistry of human brain tissue samples, surgically removed due to life-threatening contusions and/or focal brain swelling at 60.6 ± 75 hours (range 4-192 hours) postinjury in 10 severe TBI patients (age 51.7 ± 18.5 years). Control brain tissue was obtained postmortem from 5 age-matched patients without CNS disorders. TUNEL and CC1 co-labeling was used to analyze apoptotic OLs, which were increased in injured brain tissue (p < 0.05), without correlation with time from injury until surgery. The OPC markers Olig2, A2B5, NG2, and PDGFR-α were used. In contrast to the number of single-labeled Olig2, A2B5, NG2, and PDGFR-α-positive cells, numbers of Olig2 and A2B5 co-labeled cells were increased in TBI samples (p < 0.05); this was inversely correlated with time from injury to surgery (r = -0.8, p < 0.05). These results indicate that severe focal human TBI results in OL death and increases in OPCs postinjury, which may influence white matter function following TBI. Language: en |