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Pathologically Confirmed Chronic Traumatic Encephalopathy in a 25-Year-Old Former College Football Player

Jesse Mez, MD, MS1,2; Todd M. Solomon, PhD1; Daniel H. Daneshvar, MA1,3; Thor D. Stein, MD, PhD1,4,5,6; Ann C. McKee, MD1,2,4,5,6
[+] Author Affiliations
1Alzheimer’s Disease Center, Chronic Traumatic Encephalopathy Program, Boston University School of Medicine, Boston, Massachusetts
2Department of Neurology, Boston University School of Medicine, Boston, Massachusetts
3Concussion Legacy Foundation, Waltham, Massachusetts
4US Department of Veterans Affairs, VA Boston Healthcare System, Jamaica Plain, Massachusetts
5US Department of Veterans Affairs Medical Center, Bedford, Massachusetts
6Department of Pathology, Boston University School of Medicine, Boston, Massachusetts
JAMA Neurol. 2016;73(3):353-355. doi:10.1001/jamaneurol.2015.3998.
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This case report describes a 25-year-old former college football player who had more than 10 concussions while playing football and postmortem pathologically confirmed chronic traumatic encephalopathy.

Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive head impacts.1 Presently, CTE only can be diagnosed pathologically; however, research efforts, such as the ongoing Understanding Neurological Injury and Traumatic Encephalopathy (UNITE) Study,2 are investigating ways to diagnose CTE during life. As part of the UNITE Study, a panel of clinicians, blinded to neuropathology, make retrospective clinical consensus diagnoses using published criteria, including proposed clinical research criteria for CTE.3 Here, we present an informative case from the UNITE Study.

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Neuropathological Findings of Chronic Traumatic Encephalopathy (CTE)

A, The brain showed mild ventricular dilation and hippocampal atrophy. Pathological lesions of hyperphosphorylated tau (ptau) consisting of neurofibrillary tangles, neurites, and astrocytes around small blood vessels were found at the sulcal depths of the frontal and temporal lobes. Free-floating 50-µm section immunostained for AT8 (B) and paraffin-embedded 10-µm section immunostained for AT8 (C; original magnification ×200). These ptau lesions are considered to be pathognomonic for CTE based on the preliminary National Institute of Neurological Disorders and Stroke consensus criteria for the pathological diagnosis of CTE.1,5,6 Characteristic CTE ptau pathology was also found in the parietal lobes, entorhinal cortex, anterior hippocampus, hypothalamus, nucleus basalis of Meynert, substantia nigra, locus coeruleus, and median raphe. There was no immunopositivity for amyloid-β, TAR DNA-binding protein 43, or α-synuclein.

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