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Emerging Histomorphologic Phenotypes of Chronic Traumatic Encephalopathy in American Athletes
Abstract
BACKGROUND: We define chronic traumatic encephalopathy (CTE) as a progressive neurodegenerative syndrome caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. OBJECTIVE: We present emerging histomorphologic phenotypes of CTE that we identified in our cohort of CTE cases with apolipoprotein E genotyping and causes and manners of death. METHODS: Autopsy brain tissue of 14 professional athletes and 3 high school football players was examined after unexpected deaths. Histochemical and immunohistochemical tissue staining was performed with apolipoprotein E genotyping. RESULTS: Ten of 14 professional athletes (71%) were positive for CTE: 7 of 8 football players, 2 of 4 wrestlers, and 1 boxer. One of 3 high school players manifested incipient CTE. The age range of those with CTE was 18 to 52 years; they were all male athletes. In all cases of CTE, Alzheimer-type cerebral cortical atrophy was absent; negligible to mild neocortical neuronal dropout was present. The fundamental neuropathologic feature of CTE was the topographic distribution of sparse, moderate, and frequent band-shaped, flame-shaped, small and large globose neurofibrillary tangles and neuritic threads in the cerebral cortex, subcortical nuclei/basal ganglia, hippocampus, and brainstem nuclei. Sparse to frequent diffuse amyloid plaques may accompany tauopathy and was seen in only 2 CTE cases. No α-synucleinopathy was present. All 7 CTE-positive professional athletes with known apolipoprotein E genotypes had at least 1 E3 allele comprising 5 E3/E3 (71%) and 2 E3/E4 (29%). Alcohol- and drug-related deaths, suicides, and accidental deaths were overrepresented in our CTE cohort. CONCLUSION: The emerging histomorphologic features of our CTE cohort may specify histologic criteria for CTE diagnosis, may identify emerging histologic variants of CTE and may facilitate more objective surveillance and accurate identification of sentinel CTE cases.
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In the citing paper
“Prior to 2015, there were no agreed upon neuropathological criteria for CTE, and the criteria put forward by the two research groups in the US differed [15, 16].”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [15]
In the citing paper
“The consensus panel did not adopt the four neuropathological phenotypes [15] or stages of CTE [16], and indicated that the preliminary criteria were a “first step along the path to standardizing the neuropathology of CTE” [30].”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [15]
In the citing paper
“Over the past decade, the clinical features attributed to CTE have been expanded greatly and include virtually any mental health or neurological symptom or problem present prior to death”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [15]
In the citing paper
“Prior to 2016, there were no agreed upon neuropathological criteria for CTE, and the criteria published by the 2 leading research groups in the United States differed substantially (7,14).”
From Mild Chronic Traumatic Encephalopathy Neuropathology in People With No Known Participation in Contact Sports or History of Repetitive Neurotrauma (2019) · cites this paper as [7]
In the citing paper
“In different autopsy series, the percentage of former professional American football players who have died and donated their brains to research varies from 50 % [88], 80 % [146], to 97 %) [128].”
From The neuropathology of sport (2014) · cites this paper as [146]
In the citing paper
“Although CTE was first identified in association with boxing, CTE has been diagnosed neuropathologically in American football players, professional and amateur boxers, ice hockey players, professional wrestlers, soccer players, rugby players, and a professional baseball player (Figs. 3, 4, 5, 6) [38, 65, 66, 88, 91, 127, 128, 146–148].”
From The neuropathology of sport (2014) · cites this paper as [146]
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Metadata
- Authors
- Omalu, B., Bailes, J., Hamilton, R. L., Kamboh, M. I., Hammers, J., Case, M., & Fitzsimmons, R.
- Affiliations
- West Virginia University (US)
- Corresponding author
- Omalu, Bennet
- Fitzsimmons, Robert
- Venue
- Neurosurgery
- Published
- 2011-07
- Volume
- 69
- Issue
- 1
- Pages
- 173-183
- ISSN
- 0148-396X (ISSN-L)
- OpenAlex
- W1985345440
- Cited by
- 381
- References
- 22
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 9 · 2023: 21 · 2022: 17 · 2021: 18 · 2020: 20 · 2019: 31 · 2018: 30 · 2017: 41 · 2016: 39 · 2015: 44 · 2014: 35 · 2013: 36 · 2012: 16
- FWCI
- 22.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurosurgery (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- chronic traumatic encephalopathy, histopathology, neurofibrillary tangles, tauopathy, APOE genotype, professional athletes, football players, boxing, wrestling, causes of death, autopsy brain tissue, neurodegeneration
- MeSH terms
- Adolescent, Adult, Americas, Athletic Injuries, Autopsy, Brain, Cause of Death, Humans, Male, Middle Aged, Phenotype, Cohort Studies, Cerebral Amyloid Angiopathy, Neurofibrillary Tangles, Brain Injury, Chronic, Young Adult, Plaque, Amyloid
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