Chronic traumatic encephalopathy-like abnormalities in a routine neuropathology service
Abstract
Chronic traumatic encephalopathy (CTE) has been described mainly in professional athletes and military personnel and is characterized by deposition of hyperphosphorylated tau at the depths of cortical sulci and around blood vessels. To assess CTE-like changes in a routine neuropathology service, we prospectively examined 111 brains (age 18-60 years). The presence of tau-immunoreactive deposits was staged using guidelines described by others and was correlated with the medical history. 72/111 cases were negative for CTE-like changes; 34/111 were CTE stage <1; 3/111 were CTE stage 1; and 2/111 were CTE stage 2. The combined history of head injury and alcohol and/or drug abuse was a significant predictor of any CTE-like changes. Age was also a significant predictor; most with any CTE-like changes were >40 years old. CTE-like changes were not identified at sites of contusion. Among a separate group studied retrospectively, we identified 4 cases that met full criteria for CTE. We conclude that CTE-like findings are not confined to professional athletes; the risk factors of head injury and substance abuse are similar in the routine population. However, the significance of very small hyperphosphorylated tau deposits remains to be determined. In addition, the absence of typical CTE-like deposits near contusion sites keeps open the question of pathogenesis.
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Noy et al. observed that there is no lower bound for classifying Stage I CTE pathology, so if they included tiny amounts of pathology characteristic of Stage I, an additional 34 cases were identified (30.6% of the sample); therefore, 35.1% of the total sample had some degree of mild CTE pathology.
“However, they made the important observation that there is no lower bound for classifying Stage I CTE pathology, so if they included tiny amounts of pathology characteristic of Stage I, an additional 34 cases were identified (30.6% of the sample). Therefore, of the total sample, 35.1% had some degree of mild CTE pathology.”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredIn Noy et al., only one subject had a history of sports participation, and there were three women in the sample.
“Only one subject had a history of sports participation, and there were three women in the sample.”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
The Results state that only one individual in the group without CTE-like changes was explicitly involved in sports. They also report three women among the 34 cases with minimal p-tau deposits, but the prospective study as a whole included 23 women among 111 subjects. Thus, three women is not the count for the overall sample. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIt is now well-established that the pathology of CTE is present in people with other neurodegenerative diseases, such as AD, PD, and multiple system atrophy.
“Moreover, it is now well-established that the pathology of CTE is present in people with other neurodegenerative diseases, such as AD, PD, and multiple system atrophy”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
The Introduction (page not available) reports CTE-like p-tau patterns in cases of Alzheimer disease, Parkinson disease, and multiple system atrophy. But it calls the literature sparse and describes the findings as CTE-like patterns, not established CTE pathology in people with those diseases. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThere are now several studies illustrating that CTE neuropathology, at the time of death, is limited to Stage I or less in many people.
“There are now several studies illustrating that CTE neuropathology, at the time of death, is limited to Stage I or less in many people [33, 37, 39]”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
The Discussion (page unavailable) reports that 35% of adults under 60 in this medicolegal-autopsy sample had at least minimal CTE-like changes; the Results (page unavailable) also report many cases at stage <1. The paper calls these changes CTE-like and says the significance of tiny deposits is unclear, so it does not establish that all such cases had definitive CTE neuropathology. (LLM, conf=0.83)
Experimental — accuracy not yet measuredNoy et al. identified CTE pathology, based on the staging system of McKee et al., in 4.5% (three cases of Stage I and two cases of Stage II).
“They identified CTE pathology, based on the staging system of McKee et al. [16], in 4.5% (three cases of Stage I and two cases of Stage II).”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
Noy and colleagues examined 111 brains in a routine neuropathology service in Canada for the presence of CTE pathology; subjects were between the ages of 18 and 60 and were from a non-selected community-based neuropathology referral base.
“Noy and colleagues [39] examined 111 brains in a routine neuropathology service in Canada for the presence of CTE pathology. The subjects were between the ages of 18 and 60, and they were from a non-selected community-based neuropathology referral base.”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
In Noy et al., factors associated with the presence of CTE pathology were age, history of traumatic brain injury, and substance abuse.
“Factors that were associated with the presence of CTE pathology were age, history of traumatic brain injury, and substance abuse.”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
In the Canadian series of 111 brains, only 4.5% had Stage I or Stage II CTE pathology, and there were no cases of Stage III or IV pathology; nearly one in three subjects (30.6%) had a very small amount of p-tau conceptualized as less than Stage I pathology.
“In the Canadian series of 111 brains from a community autopsy service [39], only 4.5% had Stage I or Stage II CTE pathology, and there were no cases of Stage III or IV pathology. Nearly one in three subjects (30.6%), however, had a very small amount of p-tau which was conceptualized as less than Stage I pathology.”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
In Noy et al., some cases had no known history of traumatic brain injury.
“Some of the cases had no known history of traumatic brain injury.”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
In Noy et al., there was no association between CTE pathology and psychiatric illness.
“There was no association between CTE pathology and psychiatric illness in this sample.”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [39]
CTE-consistent pathology has been reported in cases with no history of head trauma, indicating that it may be a common pathology within the general population and not specific to the aftermath of mTBI.
“It is also important to note that CTE-consistent pathology has been reported in cases with no history of head trauma, further indicating that it may be a common pathology within the general population and not specific to the aftermath of mTBI [55, 69, 89, 119].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [119]
CTE pathology has been found in a small number of people with substance abuse, temporal lobe epilepsy, amyotrophic lateral sclerosis, multiple system atrophy, and other neurodegenerative diseases who have no known participation in collision or contact sports and no known exposure to repetitive neurotrauma.
“In addition, it has been found in a small number of people with (1) substance abuse (24), (2) temporal lobe epilepsy (25), (3) amyotrophic lateral sclerosis (ALS) (26), (4) multiple system atrophy (22), and (5) other neurodegenerative diseases (23) who have no known participation in collision or contact sports and no known exposure to repetitive neurotrauma.”
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 [24]
The sample studied by Noy et al was considerably younger than our case series.
“The sample studied by Noy et al was considerably younger than our case series.”
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 [24]
Some of Noy et al's cases had no known history of even a single injury to the brain.
“Some of their cases had no known history of even a single injury to the brain.”
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 [24]
CTE pathology has been identified in women and men who do not have neurological disorders, and in people with substance abuse histories.
“CTE pathology has been identified in women (23) and men (23,24) who do not have neurological disorders, and in people with substance abuse histories (24).”
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 [24]
Noy et al examined 111 brains for CTE pathology, from adults between the ages of 18 and 60, in a routine neuropathology service in Canada.
“Noy et al examined 111 brains for CTE pathology, from adults between the ages of 18 and 60, in a routine neuropathology service in Canada (24).”
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 [24]
Only 1 subject in Noy et al's sample had a known history of contact or collision sports participation.
“Only 1 subject in their sample had a known history of contact or collision sports participation.”
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 [24]
Noy et al noted that there is no lower bound for classifying Stage I CTE pathology, so if one includes sparse pathology characteristic of Stage I, an additional 34 cases were identified (30.6% of their sample).
“However, they noted that there is no lower bound for classifying Stage I CTE pathology, so if one includes sparse pathology characteristic of Stage I, an additional 34 cases were identified (30.6% of their sample).”
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 [24]
The Canadian study by Noy et al found that small amounts of pathology were very common in their community sample.
“the Canadian study by Noy et al found that small amounts of pathology were very common in their community sample (24).”
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 [24]
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- Authors
- Noy, S., Krawitz, S., & Del Bigio, M. R.
- Affiliations
- Shared Health (CA)
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-11-04
- Volume
- 75
- Issue
- 12
- Pages
- 1145-1154
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W2548378272
- Cited by
- 70
- References
- 34
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 10 · 2022: 7 · 2021: 6 · 2020: 5 · 2019: 18 · 2018: 10 · 2017: 7
- FWCI
- 10.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- chronic traumatic encephalopathy, hyperphosphorylated tau, traumatic brain injury, alcohol abuse, drug abuse, risk factors, bruising, neuropathology
- MeSH terms
- Neuropathology, Chronic Traumatic Encephalopathy, Adolescent, Adult, Brain, Female, Humans, Male, Middle Aged, Prospective Studies, Young Adult
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