scholarly journals Chronic traumatic encephalopathy – current state of knowledge

2021 ◽  
Vol 11 (8) ◽  
pp. 86-100
Author(s):  
Łukasz Bryliński ◽  
Paulina Drożak ◽  
Martyna Drożak ◽  
Katarzyna Augustowska ◽  
Piotr Duda ◽  
...  
Keyword(s):  
Tau Protein ◽  
Behavioral Problems ◽  
Current Knowledge ◽  
Chronic Traumatic Encephalopathy ◽  
Imaging Techniques ◽  
Head Injuries ◽  
Memory Loss ◽  
Ice Hockey ◽  
Diagnostic Methods ◽  
American Football

Introduction and purpose. Chronic traumatic encephalopathy (CTE) is a tauopathy caused by repetitive, mild head injuries. It is characterized by perivascular accumulation of hyperphosphorylated tau protein in the neurons and astrocytes. CTE leads to changes in central nervous system, both on microscopic and macroscopic level. The aim of the study was to present the current knowledge on chronic traumatic encephalopathy among athletes, its predisposing factors, symptoms and consequences, as well as diagnostic methods and treatment.Description. CTE occurs among contact sport players, such as American football, ice hockey, soccer, baseball, box and MMA (mixed martial arts), as well as among soldiers and victims of domestic violence. Repetitive head injuries and long career duration increase the risk of CTE. Symptoms of chronic traumatic encephalopathy include a commonly occurring triad: cognitive disturbances, behavioral problems and mood disturbances. Other symptoms include memory loss, parkinsonism, headaches, speech and walking problems. Currently, the only diagnostic method of CTE is a posthumous detection of neuropathological markers. Methods such as detection of exosomal tau protein in plasma and imaging techniques give hope to diagnose CTE in alive patients. Treatment methods of CTE, such as LIPUS (low intensity pulsed ultrasound) therapy are currently being developed.Conclusions. Chronic traumatic encephalopathy among athletes is a serious problem that affects multiple people due to the popularity of contact sports. Thus, an emphasis should be put on prevention, raising awareness and appropriate protection of athletes through changes in regulations and improvement of protective equipment.

Repetitive Head Trauma Induces Chronic Traumatic Encephalopathy by Multiple Mechanisms

2020 ◽  
Vol 40 (04) ◽  
pp. 430-438 ◽  
Author(s):  
Jonathan D. Cherry ◽  
Katharine J. Babcock ◽  
Lee E. Goldstein
Keyword(s):  
Cognitive Deficits ◽  
Tau Protein ◽  
Chronic Traumatic Encephalopathy ◽  
Biomechanical Properties ◽  
Ice Hockey ◽  
American Football ◽  
Head Impacts ◽  
Blast Exposure ◽  
Hyperphosphorylated Tau Protein ◽  
The Brain

AbstractExposure 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.

scholarly journals Chronic Traumatic Encephalopathy: A Review

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Michael Saulle ◽  
Brian D. Greenwald
Keyword(s):  
Military Service ◽  
Clinical Presentation ◽  
Chronic Traumatic Encephalopathy ◽  
Head Injuries ◽  
Emotional Disturbances ◽  
American Football ◽  
Closed Head Injuries ◽  
Apoe4 Allele ◽  
Closed Head

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that is a long-term consequence of single or repetitive closed head injuries for which there is no treatment and no definitive pre-mortem diagnosis. It has been closely tied to athletes who participate in contact sports like boxing, American football, soccer, professional wrestling and hockey. Risk factors include head trauma, presence of ApoE3 or ApoE4 allele, military service, and old age. It is histologically identified by the presence of tau-immunoreactive NFTs and NTs with some cases having a TDP-43 proteinopathy or beta-amyloid plaques. It has an insidious clinical presentation that begins with cognitive and emotional disturbances and can progress to Parkinsonian symptoms. The exact mechanism for CTE has not been precisely defined however, research suggest it is due to an ongoing metabolic and immunologic cascade called immunoexcitiotoxicity. Prevention and education are currently the most compelling way to combat CTE and will be an emphasis of both physicians and athletes. Further research is needed to aid in pre-mortem diagnosis, therapies, and support for individuals and their families living with CTE.

scholarly journals A Closer Look into the Role of Protein Tau in the Identification of Promising Therapeutic Targets for Alzheimer’s Disease

2018 ◽  
Author(s):  
Rubayat Islam Khan ◽  
Saif Shahriar Rahman Nirzhor ◽  
Barnaly Rashid
Keyword(s):  
Disease Progression ◽  
Tau Protein ◽  
Imaging Techniques ◽  
Memory Loss ◽  
Full Time ◽  
Tau Pathology ◽  
Synaptic Loss ◽  
Beta Peptides ◽  
Severe Change

One of the most commonly known chronic neurodegenerative disorders, Alzheimer’s disease (AD), manifests the common type of dementia in 60–80% of cases. From a clinical standpoint, a patent cognitive decline and a severe change in personality, as caused by a loss of neurons, is~usually evident in AD with about 50 million people affected in 2016. The disease progression in patients is distinguished by a gradual plummet in cognitive functions, eliciting symptoms such as memory loss, and eventually requiring full-time medical care. From a histopathological standpoint, the~defining characteristics are intracellular aggregations of hyper-phosphorylated tau protein, known as neurofibrillary tangles (NFT), and depositions of amyloid β-peptides (Aβ) in the brain. The~abnormal phosphorylation of tau protein is attributed to a wide gamut of neurological disorders known as tauopathies. In addition to the hyperphosphorylated tau lesions, neuroinflammatory processes could occur in a sustained manner through astro-glial activation, resulting in the disease progression. Recent findings have suggested a strong interplay between the mechanism of Tau phosphorylation, disruption of microtubules, and synaptic loss and pathology of AD. The mechanisms underlying these interactions along with their respective consequences in Tau pathology are still ill-defined. Thus, in this review: (1) we highlight the interplays existing between Tau pathology and AD; and (2) take a closer look into its role while identifying some promising therapeutic advances including state of the art imaging~techniques.

195 Chronic Traumatic Encephalopathy (CTE): Clinical and Pathological Insights

Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 252-252
Author(s):  
Domenic P Esposito
Keyword(s):  
Mental Status ◽  
Clinical Symptoms ◽  
Chronic Traumatic Encephalopathy ◽  
Memory Loss ◽  
American Football ◽  
Football Players ◽  
Post Mortem ◽  
Clinical Dementia Rating ◽  
Progressive Dementia ◽  
Boston University

Abstract INTRODUCTION Introduction: Chronic Traumatic Ence-phalopathy (CTE) is a progressive degenerative disease of the brain found in athletes and military veterans with a history of repetitive brain trauma, including symptomatic concussions as well as asymptomatic subconcussive hits to the head. The diagnosis, at this time, can only be made by post-mortem examination of brain and is based on the presence of hyperphosphorylated tau protein andneurofibrillary tangles around small blood vessels at the depths of the cortical sulci... Originally, CTE was thought to only occur in boxers however recent research has shown that other athletes, such as American football players, are at risk for the disorder. The diagnosis of CTE was first reported by Dr Bennet Omalu in 2005..Dr Ann McKee and researchers at Boston University have reported to date on 92 of 96 former NFL players diagnosed with CTE. Clinical symptoms of CTE include memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and, eventually, progressive dementia. METHODS This presentation will concentrate on the clinical evaluation of 50 + former NFL players with suspected CTE 2 of whom were also evaluated post mortem by Dr Ann McKee and researchers at Boston University. All subjects provided detailed general medical, concussion and sub concussive event, and sports medicine histories. All subjects underwent detailed neurological examinations including mini-mental status exams, clinical dementia rating scores, and extensive neuropsychological testing. Post-mortem neuropathological examinations were performed on 2 subjects. RESULTS >Analysis of pertinent historical events, results of neurological examination, clinical mental status testing, detailed neuropsychological scoring on the 50 + subjects will be presented as well as the neuropathological results on 2 overlapping subjects. Pathological grading of the 96 players examined at autopsy will also be reviewed and coorelated with clinical grading of the 50 + patients evaluated clinically. CONCLUSION The constellation of neurological, neuropsychological and pathological findings found in this large cohort of former American football players and the neuropathological findings will be discussed.

scholarly journals A Closer Look into the Role of Protein Tau in the Identification of Promising Therapeutic Targets for Alzheimer’s Disease

2018 ◽  
Author(s):  
Rubayat Islam Khan ◽  
Saif Shahriar Rahman Nirzhor ◽  
Barnaly Rashid
Keyword(s):  
Disease Progression ◽  
Tau Protein ◽  
Imaging Techniques ◽  
Memory Loss ◽  
Full Time ◽  
Tau Pathology ◽  
Synaptic Loss ◽  
Beta Peptides ◽  
Severe Change

One of the most commonly known chronic neurodegenerative disorders is Alzheimer’s disease (AD) that manifests the common type of dementia in 60-80% of AD cases. From a clinical standpoint, a patent cognitive decline and a severe change in personality, as caused by a loss of neurons, is usually evident in AD with about 50 million people affected in 2016. The disease progression in patients is distinguished by a gradual plummet in cognitive functions, eliciting symptoms like memory loss, and eventually requiring full-time medical care. From a pathophysiological standpoint, the defining characteristics are intracellular aggregations of hyper-phosphorylated tau protein, known as neurofibrillary tangles (NFT) and depositions of amyloid β-peptides (Aβ) in the brain. The abnormal phosphorylation of tau protein is attributed to a wide gamut of neurological disorders known as tauopathies. In addition to the hyperphosphorylated tau lesions, neuroinflammatory processes could occur in a sustained manner through astro-glial activation, resulting in the disease progression. Recent findings have suggested a strong interplay between the mechanism of tau phosphorylation, disruption of microtubules, and synaptic loss and pathology of AD. The mechanisms underlying these interactions along with their respective consequences in Tau pathology are still ill-defined. Thus, in this review, (1) we highlight the interplays existing between Tau pathology and AD and, (2) take a closer look into its role while identifying some promising therapeutic advances including state of the art imaging techniques.

scholarly journals A Closer Look into the Role of Protein Tau in the Identification of Promising Therapeutic Targets for Alzheimer’s Disease

2018 ◽  
Vol 8 (9) ◽  
pp. 162 ◽  
Author(s):  
Rubayat Islam Khan ◽  
Saif Nirzhor ◽  
Barnaly Rashid
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Progression ◽  
Tau Protein ◽  
Imaging Techniques ◽  
Memory Loss ◽  
Amyloid Β ◽  
Full Time ◽  
Tau Pathology ◽  
Severe Change

One of the most commonly known chronic neurodegenerative disorders, Alzheimer’s disease (AD), manifests the common type of dementia in 60–80% of cases. From a clinical standpoint, a patent cognitive decline and a severe change in personality, as caused by a loss of neurons, is usually evident in AD with about 50 million people affected in 2016. The disease progression in patients is distinguished by a gradual plummet in cognitive functions, eliciting symptoms such as memory loss, and eventually requiring full-time medical care. From a histopathological standpoint, the defining characteristics are intracellular aggregations of hyper-phosphorylated tau protein, known as neurofibrillary tangles (NFT), and depositions of amyloid β-peptides (Aβ) in the brain. The abnormal phosphorylation of tau protein is attributed to a wide gamut of neurological disorders known as tauopathies. In addition to the hyperphosphorylated tau lesions, neuroinflammatory processes could occur in a sustained manner through astro-glial activation, resulting in the disease progression. Recent findings have suggested a strong interplay between the mechanism of Tau phosphorylation, disruption of microtubules, and synaptic loss and pathology of AD. The mechanisms underlying these interactions along with their respective consequences in Tau pathology are still ill-defined. Thus, in this review: (1) we highlight the interplays existing between Tau pathology and AD; and (2) take a closer look into its role while identifying some promising therapeutic advances including state of the art imaging techniques.

Concussion in Sport

2017 ◽  
Author(s):  
Anthony P. Kontos ◽  
Jamie McAllister-Deitrick
Keyword(s):  
Structural Damage ◽  
Sport Participation ◽  
Chronic Traumatic Encephalopathy ◽  
Ice Hockey ◽  
American Football ◽  
Return To Play ◽  
Cognitive Balance ◽  
History Of ◽  
Clinical Profiles ◽  
Rehabilitation Strategies

Concussions affect millions of athletes of all ages each year in a variety of sports. Athletes in certain sports such as American football, ice hockey, rugby, soccer, and combative sports like boxing are at higher risk for concussion. Direct or indirect mechanical forces acting on the skull and brain cause a concussion, which is a milder form of brain injury. Conventional neuroimaging (e.g., computerized tomography [CT], magnetic resonance imaging [MRI]) for concussion is typically negative. Concussions involve both neurometabolic and subtle structural damage to the brain that results in signs (e.g., loss of consciousness [LOC], amnesia, confusion), symptoms (e.g., headache, dizziness, nausea), and functional impairment (e.g., cognitive, balance, vestibular, oculomotor). Symptoms, impairment, and recovery time following concussion can last from a few days to weeks or months, based on a variety of risk factors, including younger age, female sex, history of concussion, and history of migraine. Following a concussion, athletes may experience one or more clinical profiles, including cognitive fatigue, vestibular, oculomotor, post-traumatic migraine (PTM), mood/anxiety, and/or cervical. The heterogeneous nature of concussion warrants a comprehensive approach to assessment, including a thorough clinical examination and interview; symptom inventories; and cognitive, balance, vestibular, oculomotor, and exertion-based evaluations. Targeted treatment and rehabilitation strategies including behavior management, vestibular, vision, and exertion therapies, and in some cases medication can be effective in treating the various concussion clinical profiles. Some athletes experience persistent post-concussion symptoms (PCS) and/or psychological issues (e.g., depression, anxiety) following concussion. Following appropriate treatment and rehabilitation strategies, determination of safe return to play is predicated on being symptom-free and back to normal levels of function at rest and following exertion. Certain populations, including youth athletes, may be at a higher risk for worse impairment and prolonged recovery following concussion. It has been suggested that some athletes experience long-term effects associated with concussion including chronic traumatic encephalopathy (CTE). However, additional empirical studies on the role of concussion on CTE are needed, as CTE may have multiple causes that are unrelated to sport participation and concussion.

Blood Sports in an Age of Liability

2017 ◽  
Author(s):  
Jeffrey Standen
Keyword(s):  
Head Injuries ◽  
Civil Liability ◽  
Ice Hockey ◽  
American Football ◽  
Tort Liability ◽  
Contact Sports ◽  
Criminal Convictions ◽  
Civil Lawsuits ◽  
Chronic Injuries ◽  
The Brain

This chapter examines how civil liability assessments and criminal convictions have affected the legality of blood sports. Blood sports can be divided into three categories: human versus human contests, human versus animal sports, and animal versus animal fighting. For over a century, blood sports have been under both social and legal attack, resulting in significant changes in most of the historic forms of combat worldwide. The chapter begins with an overview of the most popular violent sports today, including contact sports such as American football and ice hockey. It then considers criminal prosecutions and civil lawsuits that arise from contact sports, including the “concussion suits” filed on behalf of athletes who suffered head injuries. It also discusses the doctrine of assumption of risk in sports and concludes with an analysis of how legislative intervention can obviate private tort liability for latent, chronic injuries to the brain of players.

scholarly journals Developing methods to detect and diagnose chronic traumatic encephalopathy during life: rationale, design, and methodology for the DIAGNOSE CTE Research Project

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Michael L. Alosco ◽  
Megan L. Mariani ◽  
Charles H. Adler ◽  
Laura J. Balcer ◽  
Charles Bernick ◽  
...  
Keyword(s):  
Risk Factors ◽  
Diagnostic Criteria ◽  
Chronic Traumatic Encephalopathy ◽  
Ice Hockey ◽  
Self Report ◽  
American Football ◽  
Football Players ◽  
Blood Draw ◽  
Research Project

Abstract Background Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that has been neuropathologically diagnosed in brain donors exposed to repetitive head impacts, including boxers and American football, soccer, ice hockey, and rugby players. CTE cannot yet be diagnosed during life. In December 2015, the National Institute of Neurological Disorders and Stroke awarded a seven-year grant (U01NS093334) to fund the “Diagnostics, Imaging, and Genetics Network for the Objective Study and Evaluation of Chronic Traumatic Encephalopathy (DIAGNOSE CTE) Research Project.” The objectives of this multicenter project are to: develop in vivo fluid and neuroimaging biomarkers for CTE; characterize its clinical presentation; refine and validate clinical research diagnostic criteria (i.e., traumatic encephalopathy syndrome [TES]); examine repetitive head impact exposure, genetic, and other risk factors; and provide shared resources of anonymized data and biological samples to the research community. In this paper, we provide a detailed overview of the rationale, design, and methods for the DIAGNOSE CTE Research Project. Methods The targeted sample and sample size was 240 male participants, ages 45–74, including 120 former professional football players, 60 former collegiate football players, and 60 asymptomatic participants without a history of head trauma or participation in organized contact sports. Participants were evaluated at one of four U.S. sites and underwent the following baseline procedures: neurological and neuropsychological examinations; tau and amyloid positron emission tomography; magnetic resonance imaging and spectroscopy; lumbar puncture; blood and saliva collection; and standardized self-report measures of neuropsychiatric, cognitive, and daily functioning. Study partners completed similar informant-report measures. Follow-up evaluations were intended to be in-person and at 3 years post-baseline. Multidisciplinary diagnostic consensus conferences are held, and the reliability and validity of TES diagnostic criteria are examined. Results Participant enrollment and all baseline evaluations were completed in February 2020. Three-year follow-up evaluations began in October 2019. However, in-person evaluation ceased with the COVID-19 pandemic, and resumed as remote, 4-year follow-up evaluations (including telephone-, online-, and videoconference-based cognitive, neuropsychiatric, and neurologic examinations, as well as in-home blood draw) in February 2021. Conclusions Findings from the DIAGNOSE CTE Research Project should facilitate detection and diagnosis of CTE during life, and thereby accelerate research on risk factors, mechanisms, epidemiology, treatment, and prevention of CTE. Trial registration NCT02798185

Microglia in Alzheimer’s Disease

2020 ◽  
Vol 17 (1) ◽  
pp. 29-43 ◽  
Author(s):  
Patrick Süß ◽  
Johannes C.M. Schlachetzki
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Current Knowledge ◽  
Imaging Techniques ◽  
Amyloid Β ◽  
Disease Stage ◽  
Disease Modifying Therapy ◽  
Transcriptomic Signature

: Alzheimer’s Disease (AD) is the most frequent neurodegenerative disorder. Although proteinaceous aggregates of extracellular Amyloid-β (Aβ) and intracellular hyperphosphorylated microtubule- associated tau have long been identified as characteristic neuropathological hallmarks of AD, a disease- modifying therapy against these targets has not been successful. An emerging concept is that microglia, the innate immune cells of the brain, are major players in AD pathogenesis. Microglia are longlived tissue-resident professional phagocytes that survey and rapidly respond to changes in their microenvironment. Subpopulations of microglia cluster around Aβ plaques and adopt a transcriptomic signature specifically linked to neurodegeneration. A plethora of molecules and pathways associated with microglia function and dysfunction has been identified as important players in mediating neurodegeneration. However, whether microglia exert either beneficial or detrimental effects in AD pathology may depend on the disease stage. : In this review, we summarize the current knowledge about the stage-dependent role of microglia in AD, including recent insights from genetic and gene expression profiling studies as well as novel imaging techniques focusing on microglia in human AD pathology and AD mouse models.

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