Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy

Abstract Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribut...

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Bibliographic Details
Published in:	Brain research Vol. 1630; pp. 225 - 240
Main Authors:	Puvenna, Vikram, Engeler, Madeline, Banjara, Manoj, Brennan, Chanda, Schreiber, Peter, Dadas, Aaron, Bahrami, Ashkon, Solanki, Jesal, Bandyopadhyay, Anasua, Morris, Jacqueline K, Bernick, Charles, Ghosh, Chaitali, Rapp, Edward, Bazarian, Jeffrey J, Janigro, Damir
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier B.V 01-01-2016
Subjects:	Adolescent Adult Aged Aged, 80 and over American football Blood–brain barrier Brain - metabolism Brain - pathology Brain - surgery Brain Injury, Chronic - metabolism Brain Injury, Chronic - pathology Child Child, Preschool Cognitive decline Enzyme-Linked Immunosorbent Assay Epilepsy - metabolism Epilepsy - pathology Epilepsy - surgery Female Humans Immunohistochemistry Infant Male Middle Aged Neurology Phosphorylation Serum markers tau Proteins - metabolism Traumatic brain injury Young Adult cortex American football temporal lobe epilepsy Traumatic brain injury PT CTX phosphorylated tau protein motor vehicle accident CNS TLE central nervous system Blood–brain barrier Cognitive decline CTE NFL MVA national football league Serum markers chronic traumatic encephalopathy rTBI repetitive traumatic brain injury
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Summary:	Abstract Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control ( P <0.01) but not between CTE and TLE ( P =0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Contributed equally
ISSN:	0006-8993 1872-6240
DOI:	10.1016/j.brainres.2015.11.007