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Article ; Online: Repetitive Head Trauma Induces Chronic Traumatic Encephalopathy by Multiple Mechanisms.

Cherry, Jonathan D / Babcock, Katharine J / Goldstein, Lee E

2020 Volume 40, Issue 4, Page(s) 430–438

Abstract: Exposure to repetitive neurotrauma increases lifetime risk for developing progressive cognitive deficits, neurobehavioral abnormalities, and chronic traumatic encephalopathy (CTE). CTE is a tau protein neurodegenerative disease first identified in boxers ...

Abstract	Exposure to repetitive neurotrauma increases lifetime risk for developing progressive cognitive deficits, neurobehavioral abnormalities, and chronic traumatic encephalopathy (CTE). CTE is a tau protein neurodegenerative disease first identified in boxers and recently described in athletes participating in other contact sports (notably American football, ice hockey, rugby, and wrestling) and in military veterans with blast exposure. Currently, CTE can only be diagnosed by neuropathological examination of the brain after death. The defining diagnostic lesion of CTE consists of patchy perivascular accumulations of hyperphosphorylated tau protein that localize in the sulcal depths of the cerebral cortex. Neuronal abnormalities, axonopathy, neurovascular dysfunction, and neuroinflammation are triggered by repetitive head impacts (RHIs) and likely act as catalysts for CTE pathogenesis and progression. However, the specific mechanisms that link RHI to CTE are unknown. This review will explore two important areas of CTE pathobiology. First, we will review what is known about the biomechanical properties of RHI that initiate CTE-related pathologies. Second, we will provide an overview of key features of CTE neuropathology and how these contribute to abnormal tau hyperphosphorylation, accumulation, and spread.
MeSH term(s)	Chronic Traumatic Encephalopathy/etiology ; Chronic Traumatic Encephalopathy/metabolism ; Chronic Traumatic Encephalopathy/pathology ; Humans ; Tauopathies/etiology ; Tauopathies/metabolism ; Tauopathies/pathology ; tau Proteins/metabolism
Chemical Substances	MAPT protein, human ; tau Proteins
Language	English
Publishing date	2020-07-16
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603165-1
ISSN	1098-9021 ; 0271-8235
ISSN (online)	1098-9021
ISSN	0271-8235
DOI	10.1055/s-0040-1713620
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Article ; Online: Non-suicidal self-injury at a Canadian paediatric emergency department.

Cherry, Jonathan C / Fitzpatrick, Eleanor A / Sandila, Navjot K / Lovas, David / Hurley, Katrina F

CJEM

2024 Volume 26, Issue 4, Page(s) 259–265

Abstract: Objective: Our primary objective was to determine agreement between non-suicidal self-injury recorded at triage and during subsequent mental health assessment. The secondary objective was to describe patients who reported non-suicidal self-injury.: ... ...

Abstract	Objective: Our primary objective was to determine agreement between non-suicidal self-injury recorded at triage and during subsequent mental health assessment. The secondary objective was to describe patients who reported non-suicidal self-injury. Methods: This is a health records review of patients aged 12-18 years who had an Emergency Mental Health Triage form on their health record from an ED visit June 1, 2017-May 31, 2018. We excluded patients with diagnoses of autism spectrum disorder or schizophrenia. We abstracted data from the Mental Health Triage form, Emergency Mental Health and Addictions Service Assessment forms and Assessment of Suicide and Risk Inventory. We calculated Cohen's Kappa coefficient, sensitivity, and negative predictive value to describe the extent to which the forms agreed and the performance of triage for identifying non-suicidal self-injury. We compared the cohort who reported non-suicidal self-injury with those who did not, using t-tests, Wilcoxon rank-sum tests, and chi-square tests. Results: We screened 955 ED visits and included 914 ED visits where 558 (58.4%) reported a history of non-suicidal self-injury. There were significantly more females in the group reporting non-suicidal self-injury (82.1%, n = 458) compared to the group not reporting non-suicidal self-injury (45.8%, n = 163). Patients reporting non-suicidal self-injury did so in triage and detailed Mental Health Assessment 64.7% of the time (Cohen's Kappa Coefficient 0.6); triage had sensitivity of 71.5% (95% CI 67.3-75.4) and negative predictive value of 71.2% (95% CI 68.2-74.0). Cutting was the most common method of non-suicidal self-injury (80.3%). Conclusion: Screening at triage was moderately effective in identifying non-suicidal self-injury compared to a detailed assessment by a specialised mental health team. More than half of children and adolescents with a mental health-related concern in our ED reported a history of non-suicidal self-injury, most of which were female. This symptom is important for delineating patients' coping strategies.
MeSH term(s)	Child ; Adolescent ; Humans ; Female ; Male ; Autism Spectrum Disorder ; Canada/epidemiology ; Suicide/psychology ; Emergency Service, Hospital ; Mental Health
Language	English
Publishing date	2024-04-02
Publishing country	England
Document type	Journal Article
ISSN	1481-8043
ISSN (online)	1481-8043
DOI	10.1007/s43678-024-00657-9
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Article ; Online: Inflammation and neuronal gene expression changes differ in early versus late chronic traumatic encephalopathy brain.

Labadorf, Adam / Agus, Filisia / Aytan, Nurgul / Cherry, Jonathan / Mez, Jesse / McKee, Ann / Stein, Thor D

BMC medical genomics

2023 Volume 16, Issue 1, Page(s) 49

Abstract: Background: Our understanding of the molecular underpinnings of chronic traumatic encephalopathy (CTE) and its associated pathology in post-mortem brain is incomplete. Factors including years of play and genetic risk variants influence the extent of tau ...

Abstract	Background: Our understanding of the molecular underpinnings of chronic traumatic encephalopathy (CTE) and its associated pathology in post-mortem brain is incomplete. Factors including years of play and genetic risk variants influence the extent of tau pathology associated with disease expression, but how these factors affect gene expression, and whether those effects are consistent across the development of disease, is unknown. Methods: To address these questions, we conducted an analysis of the largest post-mortem brain CTE mRNASeq whole-transcriptome dataset available to date. We examined the genes and biological processes associated with disease by comparing individuals with CTE with control individuals with a history of repetitive head impacts that lack CTE pathology. We then identified genes and biological processes associated with total years of play as a measure of exposure, amount of tau pathology present at time of death, and the presence of APOE and TMEM106B risk variants. Samples were stratified into low and high pathology groups based on McKee CTE staging criteria to model early versus late changes in response to exposure, and the relative effects associated with these factors were compared between these groups. Results: Substantial gene expression changes were associated with severe disease for most of these factors, primarily implicating diverse, strongly involved neuroinflammatory and neuroimmune processes. In contrast, low pathology groups had many fewer genes and processes implicated and show striking differences for some factors when compared with severe disease. Specifically, gene expression associated with amount of tau pathology showed a nearly perfect inverse relationship when compared between these two groups. Conclusions: Together, these results suggest the early CTE disease process may be mechanistically different than what occurs in late stages, that total years of play and tau pathology influence disease expression differently, and that related pathology-modifying risk variants may do so via distinct biological pathways.
MeSH term(s)	Humans ; Chronic Traumatic Encephalopathy/genetics ; Chronic Traumatic Encephalopathy/metabolism ; Chronic Traumatic Encephalopathy/pathology ; tau Proteins/genetics ; tau Proteins/metabolism ; Brain/metabolism ; Inflammation/metabolism ; Transcriptome ; Membrane Proteins/genetics ; Nerve Tissue Proteins/genetics
Chemical Substances	tau Proteins ; TMEM106B protein, human ; Membrane Proteins ; Nerve Tissue Proteins
Language	English
Publishing date	2023-03-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2411865-5
ISSN	1755-8794 ; 1755-8794
ISSN (online)	1755-8794
ISSN	1755-8794
DOI	10.1186/s12920-023-01471-5
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Article: Repetitive head impacts induce neuronal loss and neuroinflammation in young athletes.

Butler, Morgane L M D / Pervaiz, Nida / Ypsilantis, Petra / Wang, Yichen / Cammasola Breda, Julia / Mazzilli, Sarah / Nicks, Raymond / Spurlock, Elizabeth / Hefti, Marco M / Huber, Bertrand R / Alvarez, Victor E / Stein, Thor D / Campbell, Joshua D / McKee, Ann C / Cherry, Jonathan D

bioRxiv : the preprint server for biology

2024

Abstract: Repetitive head impacts (RHI) sustained from contact sports are the largest risk factor for chronic traumatic encephalopathy (CTE). Currently, CTE can only be diagnosed after death and the multicellular cascade of events that trigger initial ... ...

Abstract	Repetitive head impacts (RHI) sustained from contact sports are the largest risk factor for chronic traumatic encephalopathy (CTE). Currently, CTE can only be diagnosed after death and the multicellular cascade of events that trigger initial hyperphosphorylated tau (p-tau) deposition remain unclear. Further, the symptoms endorsed by young individuals with early disease are not fully explained by the extent of p-tau deposition, severely hampering development of therapeutic interventions. Here, we show that RHI exposure associates with a multicellular response in young individuals (<51 years old) prior to the onset of CTE p-tau pathology that correlates with number of years of RHI exposure. Leveraging single nucleus RNA sequencing of tissue from 8 control, 9 RHI-exposed, and 11 low stage CTE individuals, we identify SPP1+ inflammatory microglia, angiogenic and inflamed endothelial cell profiles, reactive astrocytes, and altered synaptic gene expression in excitatory and inhibitory neurons in all individuals with exposure to RHI. Surprisingly, we also observe a significant loss of cortical sulcus layer 2/3 neurons in contact sport athletes compared to controls independent of p-tau pathology. These results provide robust evidence that multiple years of RHI exposure is sufficient to induce lasting cellular alterations that may underlie p-tau deposition and help explain the early clinical symptoms observed in young former contact sport athletes. Furthermore, these data identify specific cellular responses to repetitive head impacts that may direct future identification of diagnostic and therapeutic strategies for CTE.
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.26.586815
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Article ; Online: Tau seeding in chronic traumatic encephalopathy parallels disease severity.

Kaufman, Sarah K / Svirsky, Sarah / Cherry, Jonathan D / McKee, Ann C / Diamond, Marc I

Acta neuropathologica

2021 Volume 142, Issue 6, Page(s) 951–960

Abstract: Chronic traumatic encephalopathy (CTE), a neurodegenerative tauopathy, is associated with behavioral, mood and cognitive impairment, including dementia. Tauopathies are neurodegenerative diseases whose neuropathological phenotypes are characterized by ... ...

Abstract	Chronic traumatic encephalopathy (CTE), a neurodegenerative tauopathy, is associated with behavioral, mood and cognitive impairment, including dementia. Tauopathies are neurodegenerative diseases whose neuropathological phenotypes are characterized by distinct histopathologic features of tau pathology, which progressively deposit throughout the brain. In certain tauopathies, especially Alzheimer's disease (AD), tau deposition appears to follow brain network connections. Experimental evidence suggests that the progression of tau pathology in humans, mouse and cell models could be explained by tau seeds that adopt distinct conformations and serve as templates for their own amplification to mediate transcellular propagation of pathology. Tau seeds are efficiently detected by the induction of aggregation in cell-based "biosensors" that express tau repeat domain (RD) with a disease-associated mutation (P301S) fused to complementary fluorescent protein tags (cyan and yellow fluorescent protein). Biosensors enable quantification of tau seeding in fixed and fresh-frozen brain tissue. Phospho-tau deposition in CTE follows progressive stages (I-IV), but the relationship of seeding to this deposition is unclear. We have used an established biosensor assay to independently quantify tau seeding as compared to AT8 phospho-tau histopathology in thin sections of fixed tissues of 11 brain regions from 27 patients with CTE, 5 with other tauopathies, and 5 negative controls. In contrast to prior studies of AD, we detected tau seeding late in the course of CTE (predominantly stages III and IV). It was less anatomically prevalent than AT8-positive inclusions, which were relatively widespread. We especially observed seeding in the limbic system (amygdala, thalamus, basal ganglia), which may explain the dominant cognitive and behavior impairments that characterize CTE.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Brain/pathology ; Chronic Traumatic Encephalopathy/pathology ; Female ; Humans ; Male ; Middle Aged ; Tauopathies/pathology ; tau Proteins/metabolism
Chemical Substances	MAPT protein, human ; tau Proteins
Language	English
Publishing date	2021-10-09
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-021-02373-5
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Article ; Online: Functional evaluation of epilepsy-associated KCNT1 variants in multiple cellular systems reveals a predominant gain of function impact on channel properties.

Hinckley, Christopher A / Zhu, Zhonghua / Chu, Jen-Hwa / Gubbels, Cynthia / Danker, Timm / Cherry, Jonathan J / Whelan, Christopher D / Engle, Sandra J / Nguyen, Viet

Epilepsia

2023 Volume 64, Issue 8, Page(s) 2126–2136

Abstract: Objective: Gain of function variants in the sodium-activated potassium channel KCNT1 have been associated with pediatric epilepsy disorders. Here, we systematically examine a spectrum of KCNT1 variants and establish their impact on channel function in ... ...

Abstract	Objective: Gain of function variants in the sodium-activated potassium channel KCNT1 have been associated with pediatric epilepsy disorders. Here, we systematically examine a spectrum of KCNT1 variants and establish their impact on channel function in multiple cellular systems. Methods: KCNT1 variants identified from published reports and genetic screening of pediatric epilepsy patients were expressed in Xenopus oocytes and HEK cell lines. Variant impact on current magnitude, current-voltage relationships, and sodium ion modulation were examined. Results: We determined basic properties of KCNT1 in Xenopus oocyte and HEK systems, including the role of extra- and intracellular sodium in regulating KCNT1 activity. The most common six KCNT1 variants demonstrated strong gain of function (GOF) effects on one or more channel properties. Analysis of 36 total variants identified phenotypic heterogeneity but a strong tendency for pathogenic variants to exert GOF effects on channel properties. By controlling intracellular sodium, we demonstrate that multiple pathogenic KCNT1 variants modulate channel voltage dependence by altering the sensitivity to sodium ions. Significance: This study represents the largest systematic functional examination of KCNT1 variants to date. We both confirm previously reported GOF channel phenotypes and expand the number of variants with in vitro GOF effects. Our data provide further evidence that novel KCNT1 variants identified in epilepsy patients lead to disease through generalizable GOF mechanisms including increases in current magnitude and/or current-voltage relationships.
MeSH term(s)	Humans ; Potassium Channels, Sodium-Activated/genetics ; Gain of Function Mutation ; Mutation ; Epilepsy/genetics ; Potassium Channels/genetics ; Potassium Channels/metabolism ; Nerve Tissue Proteins/genetics
Chemical Substances	Potassium Channels, Sodium-Activated ; Potassium Channels ; KCNT1 protein, human ; Nerve Tissue Proteins
Language	English
Publishing date	2023-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	216382-2
ISSN	1528-1167 ; 0013-9580
ISSN (online)	1528-1167
ISSN	0013-9580
DOI	10.1111/epi.17648
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Article: Repetitive Head Trauma Induces Chronic Traumatic Encephalopathy by Multiple Mechanisms

Cherry, Jonathan D. / Babcock, Katharine J. / Goldstein, Lee E.

Seminars in Neurology

(Chronic Traumatic Encephalopathy)

2020 Volume 40, Issue 04, Page(s) 430–438

Series title	Chronic Traumatic Encephalopathy
Abstract	Exposure to repetitive neurotrauma increases lifetime risk for developing progressive cognitive deficits, neurobehavioral abnormalities, and chronic traumatic encephalopathy (CTE). CTE is a tau protein neurodegenerative disease first identified in boxers and recently described in athletes participating in other contact sports (notably American football, ice hockey, rugby, and wrestling) and in military veterans with blast exposure. Currently, CTE can only be diagnosed by neuropathological examination of the brain after death. The defining diagnostic lesion of CTE consists of patchy perivascular accumulations of hyperphosphorylated tau protein that localize in the sulcal depths of the cerebral cortex. Neuronal abnormalities, axonopathy, neurovascular dysfunction, and neuroinflammation are triggered by repetitive head impacts (RHIs) and likely act as catalysts for CTE pathogenesis and progression. However, the specific mechanisms that link RHI to CTE are unknown. This review will explore two important areas of CTE pathobiology. First, we will review what is known about the biomechanical properties of RHI that initiate CTE-related pathologies. Second, we will provide an overview of key features of CTE neuropathology and how these contribute to abnormal tau hyperphosphorylation, accumulation, and spread.
Keywords	chronic traumatic encephalopathy (CTE) ; concussion ; neurodegeneration ; tau protein traumatic brain injury (TBI)
Language	English
Publishing date	2020-07-16
Publisher	Thieme Medical Publishers
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	603165-1
ISSN	1098-9021 ; 0271-8235
ISSN (online)	1098-9021
ISSN	0271-8235
DOI	10.1055/s-0040-1713620
Database	Thieme publisher's database

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Article ; Online: Vascular injury is associated with repetitive head impacts and tau pathology in chronic traumatic encephalopathy.

Kirsch, Daniel / Shah, Arsal / Dixon, Erin / Kelley, Hunter / Cherry, Jonathan D / Xia, Weiming / Daley, Sarah / Aytan, Nurgul / Cormier, Kerry / Kubilus, Carol / Mathias, Rebecca / Alvarez, Victor E / Huber, Bertrand R / McKee, Ann C / Stein, Thor D

Journal of neuropathology and experimental neurology

2023 Volume 82, Issue 2, Page(s) 127–139

Abstract: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repetitive head impacts (RHI) and characterized by perivascular hyperphosphorylated tau (p-tau) deposits. The role of vascular injury, blood-brain barrier leakage, and ... ...

Abstract	Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repetitive head impacts (RHI) and characterized by perivascular hyperphosphorylated tau (p-tau) deposits. The role of vascular injury, blood-brain barrier leakage, and neuroinflammation in CTE pathogenesis is not well understood. We performed quantitative immunoassays for intercellular adhesion molecule 1 (ICAM1), vascular cellular adhesion molecule 1 (VCAM1), and C-reactive protein (CRP) within the postmortem dorsolateral frontal cortex of participants with and without a history of RHI and CTE (n = 156), and tested for associations with RHI, microgliosis, and tau pathology measures. Levels of vascular injury-associated markers ICAM1, VCAM1, and CRP were increased in CTE compared to RHI-exposed and -naïve controls. ICAM1 and CRP increased with RHI exposure duration (p < 0.01) and were associated with increased microglial density (p < 0.001) and tau pathology (AT8, p-tau396, p-tau202; p < 0.05). Histologically, there was significantly increased ICAM1 staining of the microvasculature, extracellular space, and astrocytes at the sulcal depths in high stage CTE compared to both low stage CTE and controls. Multifocal perivascular immunoreactivity for serum albumin was present in all RHI-exposed individuals. These findings demonstrate that vascular injury markers are associated with RHI exposure, duration, and microgliosis, are elevated in CTE, and increase with disease severity.
MeSH term(s)	Humans ; Chronic Traumatic Encephalopathy/pathology ; Neurodegenerative Diseases ; Vascular System Injuries/complications ; Frontal Lobe/metabolism ; Blood-Brain Barrier/pathology ; tau Proteins/metabolism
Chemical Substances	tau Proteins
Language	English
Publishing date	2023-01-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/nlac122
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Article ; Online: Field Research Is Essential to Counter Virological Threats.

Runstadler, Jonathan A / Lowen, Anice C / Kayali, Ghazi / Tompkins, S Mark / Albrecht, Randy A / Fouchier, Ron A M / Stallknecht, David E / Lakdawala, Seema S / Goodrum, Felicia D / Casadevall, Arturo / Enquist, Lynn W / Alwine, James C / Imperiale, Michael J / Schultz-Cherry, Stacey / Webby, Richard J

Journal of virology

2023 Volume 97, Issue 5, Page(s) e0054423

Abstract: The interface between humans and wildlife is changing and, with it, the potential for pathogen introduction into humans has increased. Avian influenza is a prominent example, with an ongoing outbreak showing the unprecedented expansion of both geographic ...

Abstract	The interface between humans and wildlife is changing and, with it, the potential for pathogen introduction into humans has increased. Avian influenza is a prominent example, with an ongoing outbreak showing the unprecedented expansion of both geographic and host ranges. Research in the field is essential to understand this and other zoonotic threats. Only by monitoring dynamic viral populations and defining their biology
MeSH term(s)	Animals ; Humans ; Animals, Wild ; Disease Outbreaks ; Host Specificity ; Influenza in Birds/epidemiology ; Influenza, Human/epidemiology ; Influenza, Human/prevention & control ; Pandemics ; Zoonoses/epidemiology ; Zoonoses/prevention & control
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/jvi.00544-23
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Article ; Online: Tau Pathology in Chronic Traumatic Encephalopathy is Primarily Neuronal.

Butler, Morgane L M D / Dixon, Erin / Stein, Thor D / Alvarez, Victor E / Huber, Bertrand / Buckland, Michael E / McKee, Ann C / Cherry, Jonathan D

Journal of neuropathology and experimental neurology

2022 Volume 81, Issue 10, Page(s) 773–780

Abstract: Millions of individuals are exposed to repetitive head impacts (RHI) each year through contact sports, military blast, and interpersonal violence. RHI is the major risk factor for developing chronic traumatic encephalopathy (CTE), a neurodegenerative ... ...

Abstract	Millions of individuals are exposed to repetitive head impacts (RHI) each year through contact sports, military blast, and interpersonal violence. RHI is the major risk factor for developing chronic traumatic encephalopathy (CTE), a neurodegenerative tauopathy. Recent consensus criteria defined the pathognomonic lesion in CTE as perivascular, hyperphosphorylated tau (p-tau) in neuronal aggregates. Astroglial p-tau is an inconsistent supporting feature and not in itself diagnostic of CTE. This study quantitated the spatial and cellular distribution of p-tau pathology in postmortem dorsolateral frontal cortex of 150 individuals with CTE, from ages 21 to 80 years old, without comorbid pathology. p-Tau-immunoreactive cells were quantitated in the gray matter sulcus, crest, subpial region, and within pathognomonic CTE lesions. Significantly more neuronal p-tau than astrocytic p-tau was found across all cortical regions (p < 0.0001). Sulcal astrocytic p-tau was primarily (75%, p < 0.0001) localized to subpial regions as thorn-shaped astrocytes, a form of age-related tau astrogliopathy. Neuronal p-tau was significantly associated with age, years of RHI exposure, and CTE severity; astrocytic p-tau pathology was only significantly associated with age. These findings strongly support neuronal degeneration as a driving feature of CTE and will help inform future research and the development of fluid biomarkers for the detection of neuronal degeneration in CTE.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Astrocytes/pathology ; Chronic Traumatic Encephalopathy/pathology ; Frontal Lobe/pathology ; Humans ; Middle Aged ; Neurons/pathology ; Tauopathies/pathology ; Young Adult
Language	English
Publishing date	2022-07-29
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/nlac065
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