The DOI matches its Crossref record; 123 of the 123 references it cites were found in a registry or an index.
Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy After Repetitive Head Injury
Open accessAbstract
Since the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed dementia pugilistica, and more recently, chronic traumatic encephalopathy (CTE). We review 48 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 profession althletes, 1 football player and 2 boxers. Clinically, CTE is associated with memory disturbances, behavioral and personality changes, parkinsonism, and speech and gait abnormalities. Neuropathologically, CTE is characterized by atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem, with ventricular dilatation and a fenestrated cavum septum pellucidum. Microscopically, there are extensive tau-immunoreactive neurofibrillary tangles, astrocytic tangles, and spindle-shaped and threadlike neurites throughout the brain. The neurofibrillary degeneration of CTE is distinguished from other tauopathies by preferential involvement of the superficial cortical layers, irregular patchy distribution in the frontal and temporal cortices, propensity for sulcal depths, prominent perivascular, periventricular, and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes. Deposition of beta-amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases. Chronic traumatic encephalopathy is a neuropathologically distinct slowly progressive tauopathy with a clear environmental etiology.
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“It is now well established that a large percentage of former athletes identified as having CTE neuropathology also have neuropathology associated with age related neurodegenerative diseases such as AD, PD, Lewy body disease, hippocampal sclerosis, and ALS [14, 41–44] to the extent that they meet full neuropathological criteria for an alternative, well-characterized neurodegenerative disease [16].”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [14]
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“In publications from 2005–2015, CTE has been described as a progressive neurodegenerative disease characterized by a broad and diverse range of both macroscopic and microscopic neuropathology.”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [14]
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“The clinical syndrome of CTE continues to be refined but includes behavioral, mood, and cognitive dysfunction as well as occasional motor symptoms that are typically extrapyramidal (1,2).”
From Chronic Traumatic Encephalopathy Within an Amyotrophic Lateral Sclerosis Brain Bank Cohort (2018) · cites this paper as [1]
In the citing paper
“In conclusion, the prevailing theory of CTE, often expressed in articles as fact, is that it is a distinct (1, 3, 9-11) and unique (10) neurodegenerative disease (9-13).”
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 [3]
In the citing paper
“The clinical symptoms associated with this disease were examined in case summaries throughout the twentieth century; however, the disease presentation described in these reports was inconsistent [38, 65, 92, 100, 126].”
From The neuropathology of sport (2014) · cites this paper as [126]
In the citing paper
“However, despite evidence for Ab deposition in moderate to severe TBI [94], Ab plaques have not been found in early or mild stages of CTE in young individuals [65, 66, 72, 91, 126] but occur in older subjects with CTE in association with increased age at death [128].”
From The neuropathology of sport (2014) · cites this paper as [126]
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Citations
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Metadata
- Authors
- McKee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., Santini, V. E., Lee, H.-S., Kubilus, C. A., & Stern, R. A.
- Affiliations
- Boston University (US)
- ORCID
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-07
- Volume
- 68
- Issue
- 7
- Pages
- 709-735
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- PMC
- PMC2945234
- OpenAlex
- W2081325915
- Cited by
- 2,295
- References
- 123
- Citations by year
- 2026: 47 · 2025: 77 · 2024: 95 · 2023: 106 · 2022: 117 · 2021: 143 · 2020: 186 · 2019: 184 · 2018: 160 · 2017: 179 · 2016: 178 · 2015: 183 · 2014: 176 · 2013: 189 · 2012: 115
- FWCI
- 60.65
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institute on Aging (P30AG013846, P30-AG13846))
- 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, tauopathy, repetitive head injury, boxing, professional athletes, neurofibrillary tangles, brain atrophy, amyloid plaques, memory impairment, behavioral and personality changes, neuropathology
- MeSH terms
- Adult, Aged, Aged, 80 and over, Athletic Injuries, Brain, Brain Chemistry, Female, Humans, Male, Middle Aged, Neurons, Sports, Amyloid beta-Peptides, Head Injuries, Closed, Cell Death, Disease Progression, Genetic Predisposition to Disease, Brain Injury, Chronic, Tauopathies, Apolipoprotein E4
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