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It is characterized clinically by diverse neuropsychiatric symptoms, and pathologically by variable degrees of phosphorylated tau accumulation in the brain. The evolving paradigm for the pathogenesis of CTE suggests that concussion or subconcussion from athletic participation initiates a cascade of pathologic events, encompassing neuroinflammation and protein templating with trans synaptic neurotoxicity. The end result is neurologic and Authenitc Kids Chandler Catanzarojersey neurobehavioral deterioration, often with self harm. Although these concepts warrant further investigation, the available evidence permits no conclusions as regards the pathogenesis of the reported findings. Investigations into the role of premorbid or co morbid neurodegenerative diseases has been limited to date, and in depth genetic analyses have not been performed. The role of concussion or subconcussion if any, whether and how the condition progresses over time, the extent of phosphorylated tau in clinically normal athletes, the role of phosphorylated tau as a toxic species versus an inert disease response, and whether protein templating has any in vivo relevance remain to be elucidated.

Chronic traumatic encephalopathy (CTE) is the accepted term for a pattern of phosphorylated tau (ptau) deposition in the brain that appears to differ from age related accumulations and neurodegeneration.1 According to data from the largest CTE series to date, ptau tends to occur as localized accumulations in depths of sulci and perivascular areas of the cerebral cortex, particularly frontal, temporal, and insular cortices. CTE further tends to involve cortical laminae 2 and 3, relative to AD and aging where ptau predominates in laminae 3 and 5. Extensive medial temporal lobe involvement, and involvement of the brainstem tegmentum, may also be present. Axonal varicosities in the deep cortex and subcortical white matter are variously described. The gross brain varies from markedly atrophic to normal, while cavum septum pellucidum and septal fenestrations are common findings. Staging schemes have been proposed in recent years, in an attempt to understand the kinetics of the process as a function of time and clinical manifestations.1, 2

CTE is associated with contact sports and is often considered a variation of so called dementia pugilistica (DP),3, 4, 5 a long known condition in boxers associated with neurologic decline and neurofibrillary degeneration at autopsy.6 Although generally accepted as a distinct entity, DP has been controversial since its original description, with absence of prospective data,7 surprisingly few studies with autopsy correlation5, 8, 9, 10, Youth Frostee Rucker jersey 11, 12, 13 and lack of accounting for co morbidities such as Authenitc Mens John Abraham jersey substance abuse, infection, and vascular or neurodegenerative disease.13 In the only large scale study of boxers to date, Roberts14 investigated 250 boxers from a cohort of 16 boxers in the UK and found 37 with neurological lesions, suggesting an overall prevalence of 17 Some differences between CTE and DP have been suggested in a recent review, including clinical presentation, age at onset, association with APOE genotype,8 and tendencies for neurological versus psychiatric signs, although none of Elite red Chandler Catanzarojersey these features provide a clear separation. Both CTE and DP tend to be viewed as variants of the same condition tauopathy caused by brain trauma.1

The exposure to sport along with the increase in ptau in parenchymal brain tissue has suggested head trauma as the underlying biomechanical etiology of CTE. Indeed, the recent, heightened awareness of concussion and subconcussion as potentially important15 comes from studies in National Football League (NFL) players. Rare cases of CTE have been suggested in hockey player,1 professional wrestlers, rugby players,16 soccer players,12 a professional baseball player, and a circus performer.17 The issue of CTE possibly resulting from combat related traumatic brain injury (TBI) has also been raised; however, its existence as an entity in combat veterans and potential mechanisms of injury, have yet to be confirmed.18Top of pageACCEPTED CTE PARADIGMThe gaps in the knowledge of CTE are substantial, and the collective human data, which are retrospective, and largely Elite Mens Deone Bucannon jersey based on self selected cases, permit no conclusions as yet, regarding etiology or its existence as a distinct clinicopathologic entity. Nevertheless, the CTE paradigm from TBI to neurodegeneration is generally accepted, with efforts directed more at identifying the molecular events responsible for the Authenitc Womens Chandler Catanzarojersey neurodegeneration, than confirming Authenitc Youth Bobby Massie jersey its existence.19

TBI and ConcussionThe paradigm begins with the heterogeneous, imperfectly modeled, and complex condition termed TBI. In depth reviews of TBI are available.19 Briefly, TBI most often signifies loss of consciousness and is arbitrarily termed if the loss of consciousness is up to 30 Alteration in consciousness for up to 24 or posttraumatic amnesia for up to 24 is also accepted under the mild TBI umbrella. The diagnosis of mild TBI may be entirely subjective, as it is often based on self reported neurological symptoms.20 Thus, although mild TBI is portrayed in the Mens Jonathan Cooper jersey literature as a definable condition, it encompasses a wide spectrum of potential biomechanical precursors, including nature and type of impact, directionality of acceleration deceleration phenomena, and individual susceptibilities, as well as the interpretation itself which is often subjective, and often provided by physicians and other personnel with wide variability in experience in the diagnosis of TBI. There is a tendency for to be used for military related TBI, given the spectrum from mild to severe, and for to be used in sport, in place of mild TBI.

Concussion in contact sports, either objective or subjective, is a common and inevitable accompaniment of a range of sports.21 Indeed, in high school sports in the US, the concussion rate in girls soccer is comparable with that of boys football.22 The diagnosis of concussion often presents a challenge among sports medicine physicians and athletic Authenitc Kids Deone Bucannon jersey trainers, just as mild TBI may be a challenge to the Authenitc Kids Frostee Rucker jersey medical personnel in armed conflicts. Assessment by physicians with specific expertise in concussion is ideal, although this is often not available. Codified evaluation and management Womens Chandler Catanzarojersey strategies are in progress.21

Risk factors for concussion have been only obliquely addressed in the context of CTE. Among these are history of previous concussion, number and severity of concussion, age, gender, pre existing mood disorders, pre injury learning disabilities such as attention deficit hyperactivity disorder, and history of migraines.23 Prolonged concussive symptoms or post concussive syndrome that may persist in a minority of patients for weeks or even years, adds an additional level of complexity and pathophysiological uncertainty to the concept of TBI.

It is of some passing interest that one high profile NFL football player who was determined to have some degree of ptau deposition post mortem had no documented concussions during his football career at any level prior to committing suicide at Womens Chandler Catanzarojersey the age of 43. This case tends to de emphasize the importance of concussion per se, and elevates subconcussive impact as a potential etiological Authenitc Kids John Abraham jersey factor. Regardless of the specific concussion history in athletes, however, uncertainties regarding concussion and potential biomechanical antecedents to CTE are evident, notwithstanding the certainty with which concussions are viewed as etiological in the media as well as the medical literature.24

Diffuse Traumatic Axonal Injury (DAI) and Biomechanics of ConcussionUnderstanding concussion in the acute state from the standpoint of neuropathology is problematic in that the neurological deficit is transient and without mass effect, ie, the patients survive and do not require neurosurgery, precluding pathological evaluation. The pathology and mechanics of concussion are therefore difficult to study in vivo. One study that looked at brain changes in individuals who expired from other causes shortly after concussion found evidence of axonal injury, including involvement of the fornix, suggesting similarities with DAI and involvement of memory circuitry.25 Such data, however, are Authenitc red Bobby Massie jersey Kareem Martin jersey sparse. On the other hand, studies on brain contusion, a commonly observed lesion and one that is definable based on anatomic pathology have led to the basic concept that sheer stresses, or the movement of one tissue plane over another, are necessary for parenchymal brain injury.26 As emphasized by Holbourne27 more than 70 years ago, the brain relative incompressibility and lack of rigidity necessitate shear stresses over compressive stresses and rotational acceleration over linear acceleration. One could reasonably speculate, therefore, that shear stresses, rotational acceleration, and axonal disruption or injury are the basic physical precursors to concussion.

Purely biomechanical models in primates from the 1970s and 1980s may have also shed some initial light on concussion indirectly through the characterization of DAI. In these early primate models, it was determined among other factors that acceleration in the coronal plane28 and low strain rate (prolonged interval over which acceleration occurs) favored prolonged traumatic unconsciousness, poor outcome, and DAI at necropsy.29, 30 The biomechanics of DAI may therefore follow that of concussion, albeit with more severe clinical and pathological outcome. This is also consistent with the clinical definition of DAI requiring 6 of traumatic unconsciousness,31 which differs from concussion largely on the basis of duration of the unconsciousness.

At the experimental level, the last 30 years has seen a proliferation of in vitro32 and mammalian33 trauma models, which have led to an exponential expansion of data implicating essentially all major molecular disease mechanisms. The collective data indicate that TBI and otherwise biomechanical forces acting on parenchymal brain tissue result in Elite Kids John Abraham jersey pleiotropic deleterious, biochemical sequelae, encompassing signal transduction, elaboration of toxic proteins, unfolded protein responses and ER stress, oxidative stress, dysfunction in mitochondria and energy metabolism, channelopathy effects with elaboration of pore forming molecular complexes, inflammatory cytokine production, perturbations in calcium and electrolyte metabolism, and induction of apoptosis, among other mechanisms.34, 35, 36, 37, 38, 39, 40, 41 With respect to CTE, however, these processes lead to, or otherwise facilitate, tau phosphorylation via altered kinase phosphatase metabolism,42 resulting in microtubule instability and precipitation of ptau as toxic, insoluble intraneuronal and intra astrocytic inclusions.43

CTE as a Prion DiseaseSomewhat concerning are the studies suggesting protein templating with trans synaptic transmission44 and the incorporation of the tauopathies in the lexicon of prion (or prion like) diseases. Transgenic mice overexpressing P301L tau in the entorhinal cortex, for example, demonstrate de novo wild type ptau in brain regions synaptically connected with the performant pathway.45 Further, prion like self propagating of tau appear along neuroanatomical pathways following intracerebral inoculation of experimental mice transgenic for human tau.46 Similar strain propagation of amyloid has been demonstrated with synthetic peptides, and suggested as basis for phenotypic variability to human AD.47, 48 These data taken together make a sophisticated case for spreading toxicity in a prion like Elite Womens Jonathan Cooper jersey manner. The significance of this change and the correlation between such changes and clinical signs are matters of considerable uncertainty, as more research with more rigorous prevalence data is necessary even for this preliminary assertion. This is in contrast, however, to the accepted paradigm, none of which has been objectively demonstrated in humans. The accepted paradigm indicates that head trauma per se and in particular concussion, initiates the overall process, which in turn sets in motion neuroinflammatory processes that span a large spectrum of biology. Phosphorylation of tau via pathological alteration of kinase phosphatase equilibrium subsequently occurs in brain regions vulnerable to mechanical stress. Soluble, low n phospho tau oligomers of altered conformation or then spread along neuroanatomical pathways, effect conformational changes in other phospho tau species via protein templating, and cause trans synaptic neurotoxicity, which fosters disease progression. The tendency for frontotemporal involvement by phosphorylated tau further is suggested to be the basis for complex behaviors, such as impulse control, mood, and attention, as well as the reported psychiatric manifestations of CTE. Involvement of memory pathways is suggested to disrupt episodic memory. The overall neurotoxic cascade is said to overlap with, include, or even cause, pathology of Alzheimer disease, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis.

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Top of pagePROBLEMS WITH THE CURRENT PARADIGMThe DP LiteratureThe concept for present day CTE, including the naming of the condition, is based on DP, which, while broadly accepted as a clinicopathological entity, is comprised of a relatively small number of cases with remarkably heterogeneous pathology. Moreover, the few DP cases described in the literature have been examined over many decades using differing techniques, including dyes and silver impregnation, with a minority of cases assessed via immunohistochemistry for ptau and amyloid beta.

The term drunk appeared in the medical literature in a 1928 JAMA article by Martland, in which small hemorrhages were emphasized pathologically. The first case of DP with neurofibrillary degeneration was described by Brandenberg and Hallervorden50, in a 51 year old retired boxer (retired at age 28 after 11 years as an amateur boxer), although plaque pathology and cerebral amyloid angiopathy were also noted, as was death from intracerebral hemorrhage, raising the possibility of early onset AD. Courville51 in 1962 reported an autopsy case of punch drunk syndrome, although no neurofibrillary degeneration or features presently ascribed to CTE were mentioned. Constantinides and Tissot in 196752 described severe degeneration of the substantia nigra with numerous neurofibrillary tangles in a 58 year old man who had been retired from boxing for 34 years,5 raising the possibility of co morbid tauopathy. Payne11 in 1968 described autopsy findings in six boxers in their forties, calling attention to septal abnormalities. CTE changes according to modern concepts (perivascular and superficial neurofibrillary change, neurofibrillary change in the depth of sulci) were not apparent, although neurofibrillary changes were observed in two brains, and were considered non specific.

The largest series to date, however, was that of Corsellis et al,5 who described findings in 15 boxers. In this seminal article, neurofibrillary degeneration out of proportion to plaque pathology was established as an integral pathological change, while also emphasizing septal changes, substantia nigra degeneration, and cerebellar scarring. Clinical findings often included speech abnormalities, ataxia, and movement disorders. A closer look at the cases, however, indicates a level of complexity and variability. At least 6 of the 15 cases were accompanied by heavy alcohol use. Co morbidities such as hypertensive vascular disease with lacunar infarcts were evident in some cases. One patient had tabes dorsalis, another had a cavernous malformation of the globus pallidus, while others had little pathology and were neurologically normal during life. A number of the subjects boxed in the early part of the twentieth century, when several hundred fights were not uncommon. Atrophy involving hypothalamus and mammillary bodies in some of these cases warrants discussion of thiamine deficiency and Wernicke syndrome. It should also be noted, in light of the recently identified genetic lesions that cause FTLD family history was not commented upon in any of the cases in this series. Thus, although the description of neurofibrillary degeneration was remarkable, the limited numbers, extensive head trauma exposure, and co morbidities indicate a level of uncertainty even in the relatively well accepted entity of DP.

More recent cases are fewer but perhaps more compelling. For example, Hof et al55 described neurofibrillary tangle clusters in frontal and temporal cortices in a 24 year old autistic patient who was prone to frequent and protracted self injurious head banging. The findings included a tendency for focal involvement of cortical laminae 2 and 3, now considered a feature of CTE. Geddes et al12 noted neurofibrillary change with a tendency for basal cortical involvement by tau immunohistochemistry in two boxers in their twenties, and further called Womens Chandler Catanzarojersey attention to perivascular tau, also considered a hallmark of CTE. Neither subject had clinical signs suggesting DP, however. About the same time, the New England Journal of Medicine presented a case of multisystem neurodegenerative disease, including involvement of the spinal cord and substantia nigra, in a 67 year old retired boxer (10 year career with over 100 bouts).56 Interestingly, probable amyotrophic lateral sclerosis was diagnosed in the patient brother, raising the possibility of pathogenic mutation. Schmidt et al57 examined brain tissue from this same patient and one additional retired boxer, aged 78, and noted that the tau isoform profile in soluble fractions resembled that of AD. The second patient, however, had Lewy bodies in the substantia nigra, again raising the issue of co morbid neurodegenerative disease. Areza Fegyveres et al58 reported a case of DP with a clinical progression that was indistinguishable from AD. He had fought more than 60 bouts but had never been knocked out.

McKee and colleagues on the other hand more Authenitc Womens Jonathan Cooper jersey than doubled the cases of sport associated tauopathy reported in the literature with a remarkable brain procurement effort, particularly targeting NFL athletes.1 Emphasis was placed on the pattern of tauopathy, best illustrated by thick, sledge microtome whole mount immunostains. Thus, the updated pathology of CTE includes: (i) localized neuronal and glial accumulations of phosphorylated tau involving perivascular areas of the cerebral cortex, sulcal depths, and with a preference for neurons within superficial cortical laminae; (ii) multifocal axonal varicosities involving deep cortex and subcortical white matter; (iii) relative lack of A deposits; and (iv) TDP 43 positive inclusions and neurites. The first of the above findings is Elite red Frostee Rucker jersey arguably the most robust, as these distributions are generally not described as incidental accumulations with age or as a prominent feature in AD. Axonal varicosities, relative lack of A and TDP 43 pathology may be difficult to distinguish from other diseases and controls in blinded analyses.

In a review of the CTE (including DP) literature to date, however, Gardner et al8 noted that of the 61 pure athlete cases reported by McKee et al, 25 demonstrated no pathological features of CTE, and 25 had CTE pathology. Of those with pure CTE pathology, clinical findings were sometimes absent or nonspecific. Noteworthy also was that only a minority of cases showed disease progression, contrary to the commonly held view that CTE is a neurodegenerative disease.

Both DP as classically defined, and modern day CTE, therefore span a wide spectrum from normal to advanced disease, from the standpoint of both clinical presentation and neuropathological findings, with disease progression being doubtful in many cases according to one review. The broad question of whether DP or CTE merits inclusion in the broad category of neurodegenerative disease may be debated in light of these data, although the low thresholds for expIt is characterized clinically by diverse neuropsychiatric symptoms, and pathologically by variable degrees of phosphorylated tau accumulation in the brain. The evolving paradigm for the Elite Womens Bobby Massie jersey pathogenesis of CTE suggests that concussion or subconcussion from athletic participation initiates a cascade of pathologic events, encompassing neuroinflammation and protein templating with trans synaptic neurotoxicity. The end result is neurologic and neurobehavioral deterioration, often with self harm. Although these concepts warrant further investigation, the available evidence permits no conclusions as regards the pathogenesis of the reported findings. Investigations into the role of premorbid or co morbid neurodegenerative diseases has been limited to date, and in depth genetic analyses have not been performed. The role of concussion or subconcussion if any, whether and how the condition progresses over time, the extent of phosphorylated tau in clinically normal athletes, the role of phosphorylated tau as a toxic species versus an inert disease response, and whether protein templating has any in vivo relevance remain to be elucidated.

Chronic traumatic encephalopathy (CTE) is the accepted term for a pattern of phosphorylated tau (ptau) deposition in the brain that appears to differ from age related accumulations and neurodegeneration.1 According to data from the largest CTE series to date, ptau tends to occur as localized accumulations in depths of sulci and perivascular areas of the cerebral cortex, particularly frontal, temporal, and insular cortices. CTE further tends to involve cortical laminae Kareem Martin jersey 2 and 3, relative to AD and aging where ptau predominates in laminae 3 and 5. Extensive medial temporal lobe involvement, and involvement of the brainstem tegmentum, may also be present. Axonal varicosities in the deep cortex and subcortical Youth John Abraham jersey white matter are variously described. The gross brain varies from markedly atrophic to normal, while cavum septum pellucidum and septal fenestrations are common findings. Staging schemes have been proposed in recent years, in an attempt to understand the kinetics of the process as a function of time and clinical manifestations.1, 2

CTE is associated with contact sports and is often considered a variation of so called dementia pugilistica (DP),3, Authenitc John Abraham jersey 4, 5 a long known condition in boxers associated with neurologic decline and neurofibrillary degeneration at autopsy.6 Although generally accepted as a distinct entity, DP has been controversial since its original description, with absence of prospective data,7 surprisingly few studies with autopsy correlation5, 8, 9, 10, 11, 12, 13 and lack of accounting for co morbidities such as substance abuse, infection, and vascular or neurodegenerative disease.13 In the only large scale study of boxers to date, Roberts14 investigated 250 boxers from a cohort of 16 boxers in the UK and found 37 with neurological lesions, suggesting an overall prevalence of 17 Some differences between CTE and DP have been suggested in a recent review, including clinical presentation, age at onset, association with APOE genotype,8 and tendencies for neurological versus psychiatric signs, although none of these features provide a clear separation. Both CTE and DP tend to be viewed as variants of the same condition tauopathy caused by brain trauma.1

The exposure to sport along with the increase in ptau in parenchymal brain tissue has suggested head trauma as the underlying biomechanical etiology of CTE. Indeed, the recent, heightened awareness of concussion and subconcussion as potentially important15 comes from studies in National Football League (NFL) players. Rare cases of CTE have been suggested in hockey player,1 professional wrestlers, rugby players,16 soccer players,12 a professional baseball player, and a circus performer.17 The issue of CTE possibly resulting from Elite Youth John Abraham jersey combat related traumatic brain injury (TBI) has also been raised; however, its existence as an entity in combat veterans and potential mechanisms of injury, have yet to be confirmed.18Top of pageACCEPTED CTE PARADIGMThe gaps in the knowledge of CTE are substantial, and the collective human data, which are retrospective, and largely based on self selected cases, permit no conclusions as yet, regarding etiology or its existence as a distinct clinicopathologic entity. Nevertheless, the CTE paradigm from TBI to neurodegeneration is generally accepted, with efforts directed more at identifying the molecular events responsible for the neurodegeneration, than confirming its existence.19

TBI and ConcussionThe paradigm begins with the heterogeneous, imperfectly modeled, and complex condition termed TBI. In depth reviews of TBI are available.19 Briefly, TBI most often signifies loss of consciousness and is arbitrarily termed if the loss of consciousness is up to 30 Alteration in consciousness for up to 24 or posttraumatic amnesia for up to 24 is also accepted under Elite Kids Jonathan Cooper jersey the mild TBI umbrella. The diagnosis of mild TBI may be Elite red Jonathan Cooper jersey entirely subjective, as it is often based on self reported neurological symptoms.20 Thus, although mild TBI is portrayed in the literature as a definable condition, it encompasses a wide spectrum of potential biomechanical precursors, including nature and type of impact, directionality of acceleration deceleration phenomena, and individual susceptibilities, as well as the interpretation itself which is often subjective, and often provided by physicians and other personnel with wide variability in experience in the diagnosis of TBI. There is a tendency for to be used for military related TBI, given the spectrum from mild to severe, and for to be used in sport, in place of Authenitc Kids Chandler Catanzarojersey mild TBI.

Concussion in contact sports, either objective or subjective, is a common and inevitable accompaniment of a range of sports.21 Indeed, in high school sports in the US, the concussion rate in girls soccer is comparable with that of boys football.22 The diagnosis of concussion often presents a challenge among sports medicine physicians and athletic trainers, just as mild TBI may be a challenge to the medical personnel in armed conflicts. Assessment by physicians with specific expertise in concussion is ideal, although this is often not available. Codified evaluation and management strategies are in progress.21

Risk factors for concussion have been only obliquely addressed in the context of CTE. Among these are history of previous concussion, number and severity of concussion, age, gender, pre existing mood disorders, pre injury learning disabilities such as attention deficit hyperactivity disorder, and history of migraines.23 Prolonged concussive symptoms or post concussive syndrome that may persist in a minority of patients for weeks or even years, adds an additional level of complexity and pathophysiological uncertainty to the concept of TBI.

It Authenitc red Deone Bucannon jersey is of some passing interest that one high profile NFL football player who was determined to have some degree of ptau deposition post mortem had no documented concussions during his football career at any level prior to committing suicide at the age of 43. This case tends to de emphasize the importance of concussion per se, and elevates subconcussive impact as a potential etiological factor. Regardless of the specific concussion history in athletes, however, uncertainties regarding concussion and potential biomechanical antecedents to CTE are evident, notwithstanding the certainty with which concussions are viewed as etiological in the media as well as the medical literature.24

Diffuse Traumatic Axonal Injury (DAI) and Biomechanics of ConcussionUnderstanding concussion in the acute state from the standpoint of neuropathology is problematic in that the neurological deficit is transient and without mass effect, ie, the patients survive and do not require neurosurgery, precluding pathological evaluation. The pathology and mechanics of concussion are therefore difficult to study in vivo. One study that looked at brain changes in individuals who expired from other causes shortly after concussion found evidence of axonal injury, Authenitc Mens Deone Bucannon jersey including involvement of the fornix, suggesting similarities with DAI and involvement of memory circuitry.25 Such data, however, are sparse. On the other hand, studies on brain contusion, a commonly observed lesion and one that is definable based on anatomic pathology have led to the basic concept that sheer stresses, or the movement of one tissue plane over another, are necessary for parenchymal brain injury.26 As emphasized by Holbourne27 more than 70 years ago, the brain relative incompressibility and lack of rigidity necessitate shear stresses over compressive stresses and rotational acceleration over linear acceleration. One could reasonably speculate, therefore, that shear stresses, rotational acceleration, and axonal disruption or injury are the basic physical precursors to concussion.

Purely biomechanical models in primates from the 1970s and 1980s may have also shed some initial light on concussion indirectly through the characterization of DAI. In these early primate models, it was determined among other factors that acceleration in the coronal plane28 and low strain rate (prolonged interval over which acceleration occurs) favored prolonged traumatic unconsciousness, poor outcome, and DAI at necropsy.29, 30 The biomechanics of DAI may therefore follow that of concussion, albeit with more severe clinical and pathological outcome. This is also consistent with the clinical definition of DAI requiring 6 of traumatic unconsciousness,31 which differs from concussion largely on the basis of duration of Elite Youth Deone Bucannon jersey the unconsciousness.

At the experimental level, the last 30 years has seen a proliferation of in vitro32 and mammalian33 trauma models, which have led to an exponential expansion of data implicating essentially all major molecular disease mechanisms. The collective data indicate that TBI and otherwise biomechanical forces acting on parenchymal brain tissue result in pleiotropic deleterious, biochemical sequelae, encompassing signal transduction, elaboration of toxic proteins, unfolded protein responses and ER stress, oxidative stress, dysfunction in mitochondria and energy metabolism, channelopathy effects with elaboration of pore forming molecular complexes, inflammatory cytokine production, perturbations in calcium and electrolyte metabolism, and induction of apoptosis, among other mechanisms.34, 35, 36, 37, 38, 39, 40, 41 With respect to CTE, however, these processes lead to, or otherwise facilitate, tau phosphorylation via altered kinase phosphatase metabolism,42 resulting in microtubule instability and precipitation of ptau as toxic, insoluble intraneuronal and intra astrocytic inclusions.43

CTE as a Prion DiseaseSomewhat concerning are the studies suggesting protein templating with trans synaptic transmission44 and the incorporation of the tauopathies in the lexicon of prion (or prion like) diseases. Transgenic mice overexpressing P301L tau in the entorhinal cortex, for example, demonstrate de novo Authenitc Youth Frostee Rucker jersey wild type ptau in brain regions synaptically connected with the performant pathway.45 Further, prion like self propagating of tau appear along neuroanatomical pathways following intracerebral inoculation of experimental mice transgenic for human tau.46 Similar strain propagation of amyloid has been demonstrated with synthetic peptides, and suggested as basis for phenotypic variability to human AD.47, 48 These data taken together make a sophisticated case for spreading toxicity in a prion like manner. The significance of this change and the correlation between such changes and clinical signs are matters of considerable uncertainty, as more research with more rigorous prevalence data is necessary even for this preliminary assertion. This Kids Frostee Rucker jersey is in contrast, however, to the accepted Womens Deone Bucannon jersey paradigm, none of which has been objectively demonstrated in humans. The accepted paradigm indicates that head trauma per se and in particular concussion, initiates the overall process, which in turn sets in motion neuroinflammatory processes that span a large spectrum of biology. Phosphorylation of tau via pathological alteration of kinase phosphatase equilibrium subsequently occurs in brain regions vulnerable to mechanical stress. Soluble, low n phospho tau oligomers of altered conformation or then spread along neuroanatomical pathways, effect conformational changes in other phospho tau species via protein templating, and cause trans synaptic neurotoxicity, which fosters disease progression. The tendency for Authenitc John Abraham jersey frontotemporal involvement by phosphorylated tau further is suggested to be the basis for complex behaviors, such as impulse control, mood, and attention, as well as the reported psychiatric manifestations of CTE. Involvement of memory pathways is suggested to disrupt episodic memory. The overall neurotoxic cascade is said to overlap with, include, or even cause, pathology of Alzheimer disease, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis.

Full figure and legend (59K)

Top of pagePROBLEMS WITH THE CURRENT PARADIGMThe DP LiteratureThe concept for present day CTE, including the naming of the condition, is based on DP, which, while broadly accepted as a clinicopathological entity, is comprised of a relatively small number of cases with remarkably heterogeneous pathology. Moreover, the few DP cases described in the literature have been examined over many decades using differing techniques, including dyes and silver impregnation, with a minority of cases assessed via immunohistochemistry for ptau and amyloid beta.

The term drunk appeared in the medical literature in a 1928 JAMA article by Martland, in which small hemorrhages were emphasized pathologically. The first case of DP with neurofibrillary degeneration was described by Brandenberg and Hallervorden50, in a 51 year old retired boxer (retired at age 28 after 11 years as an amateur boxer), although plaque pathology and cerebral amyloid angiopathy were also noted, as was death from intracerebral hemorrhage, raising the possibility of early onset AD. Courville51 in 1962 reported an autopsy case of punch drunk syndrome, although no neurofibrillary degeneration or features presently ascribed to CTE were mentioned. Constantinides and Tissot in 196752 described severe degeneration of the substantia nigra with numerous neurofibrillary tangles in a 58 year old man who had been retired from boxing for 34 years,5 raising the possibility of co morbid tauopathy. Payne11 in 1968 described autopsy findings in six boxers in their forties, calling attention to septal abnormalities. CTE changes according to modern concepts (perivascular and superficial neurofibrillary change, neurofibrillary change in the depth of sulci) were not apparent, although neurofibrillary changes were observed in two brains, and were considered non specific.

The largest series to date, Frostee Rucker jersey however, was that of Corsellis et al,5 who described findings in 15 boxers. In this seminal article, neurofibrillary degeneration out of proportion to plaque pathology was established as an integral pathological change, while also emphasizing septal changes, substantia nigra degeneration, and cerebellar scarring. Clinical findings often included speech abnormalities, ataxia, and movement disorders. A closer look at the cases, however, indicates a level of complexity and variability. At least 6 of the 15 cases were accompanied by heavy alcohol use. Co morbidities such as hypertensive vascular disease with lacunar infarcts were evident in some cases. One patient had tabes Authenitc red Frostee Rucker jersey dorsalis, another had a cavernous malformation of the globus pallidus, while others had little pathology and were neurologically normal during life. A number of the subjects boxed in the early part of the twentieth century, when several hundred fights were not uncommon. Atrophy involving hypothalamus and mammillary bodies Elite red Bobby Massie jersey in some of these cases warrants discussion of thiamine deficiency and Wernicke syndrome. It should also be noted, in light of the recently identified genetic lesions that cause FTLD family history was not commented upon in any of the cases in this series. Thus, although the description of neurofibrillary degeneration was remarkable, the limited numbers, extensive head trauma exposure, and co morbidities indicate a level of uncertainty even in the relatively well accepted entity of DP.

More recent cases are fewer but perhaps more compelling. For example, Hof et al55 described neurofibrillary tangle clusters in frontal and temporal cortices in Kids John Abraham jersey a 24 year old autistic patient who was prone to frequent and protracted self injurious head banging. The findings included a tendency for focal involvement of cortical laminae 2 and 3, now considered a feature of CTE. Geddes et al12 noted neurofibrillary change with a tendency for basal cortical involvement by tau immunohistochemistry in two boxers in their twenties, and further called attention to perivascular tau, also considered a hallmark of CTE. Neither subject had clinical signs suggesting DP, however. About the same time, the New England Journal of Medicine presented a case of multisystem neurodegenerative disease, including involvement of the spinal cord and substantia nigra, in a 67 year Elite Chandler Catanzaro jersey old retired boxer (10 year career with over 100 bouts).56 Interestingly, probable amyotrophic lateral sclerosis was diagnosed in the patient brother, raising the possibility of pathogenic mutation. Schmidt et al57 examined brain tissue from this same patient and one additional retired boxer, aged 78, and noted that the tau isoform profile in soluble fractions resembled that of AD. The second patient, however, had Lewy bodies in the substantia nigra, again raising the issue of co morbid neurodegenerative disease. Areza Fegyveres et al58 reported a case of DP with a clinical progression that was indistinguishable from AD. He had fought more than 60 bouts but had never been knocked out.

McKee and colleagues on the other hand more than doubled the cases of sport associated tauopathy reported in the literature with a remarkable brain procurement effort, particularly targeting NFL athletes.1 Emphasis was placed on the pattern of tauopathy, best illustrated by thick, sledge microtome whole mount immunostains. Thus, the updated pathology of CTE includes: (i) localized neuronal and glial accumulations of phosphorylated tau involving perivascular areas of the cerebral cortex, sulcal depths, and with a preference for neurons within superficial cortical laminae; (ii) multifocal axonal varicosities involving deep cortex and subcortical white matter; (iii) relative lack of A deposits; and (iv) TDP 43 positive inclusions and neurites. The first of the above findings is arguably the most robust, as these distributions are generally not described as incidental accumulations with age or as a prominent feature in AD. Axonal varicosities, relative lack of A and TDP 43 pathology may be difficult to distinguish from other diseases and controls in blinded analyses.

In a review of the CTE (including DP) literature to date, however, Gardner et al8 noted that of the 61 pure athlete cases reported by McKee et al, 25 demonstrated no pathological features of CTE, and 25 had CTE pathology. Of those with pure CTE pathology, clinical findings were sometimes absent or nonspecific. Noteworthy also was that only a minority of cases showed disease progression, contrary to the commonly held view that CTE is a neurodegenerative disease.

Both DP as classically defined, and modern day CTE, therefore span a wide spectrum from normal to advanced disease, from the standpoint of both clinical presentation and neuropathological findings, with disease progression being doubtful in many cases according to one review. The broad question of whether DP or CTE merits inclusion in the broad category of neurodegenerative disease may be debated in light of these data, although the low thresholds for exp

Byline: Norman Chad

The Indianapolis Colts are one step away from the Super Bowl, which is akin to Mister Ed being one step away from the Kentucky Derby.

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I mean, who are these guys?

Here’s a test for you:

Group A: Stephen Grant, Quentin Coryatt, Tony McCoy, Jeff Herrod, Bernard Whittington, Ray Buchanan, Conrad Clarks.

Group B: Eddie White, Nathan Clifford, John McLean, James Wilson, Thomas Todd, Stanley Reed, Tom Clark.

One of those groups are former Supreme Court justices and one of those groups are current Indianapolis Colts defensive players.

Answer: Group A wears helmets, Group B wears robes.

Even on offense, the only Colt any of us ever has heard of is Jim Harbaugh, and you have to figure if Harbaugh gets hurt, they’ll probably bring in Earl Morrall.

(Incidentally, a recent survey revealed that seven of 29 NFL owners had not ever realized the Colts Elite Mens Bobby Massie jersey were no longer in Baltimore. Al Kids Chandler Catanzaro jersey Davis was not included in the survey, because none of the acceptable responses to the question asked provided for profanity.)

Curiously, Indianapolis is the 24th largest TV market in the country, but when adjusted for black and white sets and homes not tuned Authenitc Jonathan Cooper jersey to ESPN’s «SpeedWeek,» it falls Kids John Abraham jersey to No. 172.

(By the way, Elite Womens Chandler Catanzarojersey NBC announced Elite Youth John Abraham jersey that, in the event the Colts win today, it will Authenitc red Frostee Rucker jersey pre empt its entire Super Bowl XXX coverage Jan. 28 to air a «Best of ‘Blossom’ » retrospective.)

We can kid Indianapolis because we love Indianapolis. And, in this continually improbable NFL season, I’ll stand Elite Womens Deone Bucannon jersey somewhat firm in support of the Colts. The Steelers are 11 point favorites Jonathan Cooper jersey in Pittsburgh. Pittsburgh will win but Indianapolis will cover. Pick: Colts.

Packers at Cowboys ( 9): This is the Good Ship Lollipop vs. the Evil Empire. This is a publicly owned team vs. a privately held monolith. This is everything good and clean and pure and Elite John Abraham jersey right in America vs. dirty, stinkin’ scoundrels.

I think you know where The Man stands on this one.

I have a message for Jerry and Deion and Troy and Michael and Emmitt: Sure, you’re good at Elite red Deone Bucannon jersey what you do, but you’ve been on stage a bit too long. In that manner, Cowboys games are very much like Howie Mandel concerts.

We here in Mens Frostee Rucker jersey Green Bay well, technically, I’ve never been to Wisconsin, although I now list Sheboygan as my hometown for football and Authenitc Mens Bobby Massie jersey social reasons believe the Packers have the better quarterback (Brett Favre), the better coach (Mike Holmgren), the better cause (restoring pride to Titletown USA) and the better God fearing defensive lineman (Reggie White).

Heck, the last time Charles Haley went to church, he sacked the altar boy.

Meanwhile, on the subject of sex, raised by the Cowboys’ Nate Newton on Monday, the 320 pound guard actually said he Authenitc Kids John Abraham jersey warned his teammates to abstain «anywhere from 24 to 48 hours» before Elite Kids Chandler Catanzarojersey Elite Mens Chandler Catanzarojersey last week’s Eagles game and, this week, «I’m trying to hold it to 72 hours.» Frankly, I don’t think Bill Bates and you all have seen him on special teams as long as I have, folks can go that long without some type of physical contact.

(Personal Note: The Man generally abstains from sex from 24 to 48 days before columns, but this Elite Jonathan Cooper jersey is not so much a standing rule as it is sad reality.

As we all know by now, the Cowboys have beaten the Packers five times in the past three seasons, all in Dallas, twice in the playoffs. To which I say, after deep and penetrating analysis:The Cowboys are going down, like the plundering Visigoths did in the eighth century. And if they don’t, I’ll be back in two weeks to tell you why they’re going down in Super Bowl XXX. Pick: Packers.

Last week: 2 2.( Quick Gambling Yarn: Week after week, a gambler was losing his shirt on football. Each Saturday he’d bet on college games and each Sunday he’d bet on NFL games and each weekend he’d lose a bundle. He was the bookie’s dream. Then the football season neared an end, and the bookie was upset because of his anticipated loss of revenue. How, he wondered, could he keep this losing customer? Finally, he went to the guy and said, «Listen, hockey season is under way and we’ll be happy to take your action.» «Hockey,» said the man, insulted.Byline: Norman Chad

The Indianapolis Colts are one step away from the Super Bowl, which is akin to Mister Ed being Authenitc Mens Deone Bucannon jersey one step away from the Kentucky Derby.

The Indianapolis Colts? As of two weeks ago, I honestly could not have named a single Colts defensive starter. In Miami once, they had the No Name Defense, but in Indianapolis, we’re talking No DNA Defense.

I mean, who are these guys?

Here’s a test for you:

Group A: Stephen Grant, Quentin Mens John Abraham jersey Coryatt, Tony McCoy, Jeff Herrod, Bernard Whittington, Ray Buchanan, Conrad Clarks.

Group B: Eddie White, Nathan Clifford, John McLean, James Wilson, Thomas Todd, Stanley Reed, Tom Clark.

One of those groups are former Supreme Court justices and one of those groups are current Indianapolis Colts defensive players.

Answer: Group A wears helmets, Group B wears robes.

Even on offense, Youth Deone Bucannon jersey the only Colt any of us ever has heard of is Jim Harbaugh, and you have to figure if Harbaugh gets hurt, they’ll probably bring in Earl Morrall.

(Incidentally, a recent survey revealed that seven of 29 Womens Frostee Rucker jersey NFL owners had not ever realized the Colts were no longer in Baltimore. Authenitc red Bobby Massie jersey Al Davis was not included in the survey, Elite Mens Chandler Catanzarojersey Kareem Martin jersey because none of the acceptable responses to the question asked provided for profanity.)

Curiously, Indianapolis is the Elite red Jonathan Cooper jersey 24th largest TV market in the country, but when adjusted for black and white sets Youth John Abraham jersey and homes not tuned to ESPN’s «SpeedWeek,» it falls to No. 172.

(By the way, NBC announced that, in the event the Colts win today, it will pre empt its entire Super Bowl XXX coverage Jan. 28 to air a «Best of ‘Blossom’ » retrospective.)

We can kid Indianapolis because we love Indianapolis. And, in this continually improbable NFL season, I’ll stand somewhat firm in support of the Colts. The Steelers are 11 point favorites in Pittsburgh. Pittsburgh will win but Indianapolis will cover. Pick: Colts.

Packers at Cowboys ( 9): This is the Good Ship Lollipop vs. the Evil Empire. This is a Elite red Frostee Rucker jersey publicly owned team vs. Authenitc Womens Bobby Massie jersey a privately Jonathan Cooper jersey held monolith. This is everything good and clean and pure and right in America vs. dirty, stinkin’ scoundrels.

I Mens Chandler Catanzarojersey think you know where The Man stands on this one.

I have a message for Jerry and Deion and Troy and Michael and Emmitt: Sure, you’re good at what you do, but you’ve been Authenitc John Abraham jersey on stage a bit too long. In that manner, Cowboys games are very much like Howie Mandel concerts.

We here in Green Bay well, technically, I’ve never been to Wisconsin, although I now list Sheboygan as my hometown for football and Authenitc Youth Authenitc Youth John Abraham jersey Deone Bucannon jersey social reasons believe the Packers have the better quarterback (Brett Favre), Youth Chandler Catanzarojersey the better coach (Mike Holmgren), the better cause (restoring pride to Titletown USA) and the better God fearing defensive lineman (Reggie White).

Heck, the last time Charles Haley went to church, he sacked Elite Youth Jonathan Cooper jersey the altar boy.

Meanwhile, on the subject of sex, raised by the Cowboys’ Nate Newton on Monday, the 320 pound guard actually said he warned his teammates to abstain «anywhere from 24 to 48 hours» before last week’s Eagles game and, this week, «I’m trying to hold it to 72 hours.» Frankly, I don’t think Bill Bates and you all have seen him on special teams as long as I have, folks can go that long without some type of physical contact.

(Personal Note: The Man generally abstains from sex from 24 to 48 days before columns, but this is not so much a standing rule as it is sad reality.

As we all know by now, the Cowboys have beaten the Packers five times in the past three seasons, all in Dallas, twice in the playoffs. To which I Authenitc Youth Chandler Catanzarojersey say, after deep and penetrating analysis:The Cowboys are going down, like the plundering Visigoths did in the eighth century. And if they don’t, I’ll be back in two weeks to tell you why they’re going down in Super Bowl XXX. Pick: Packers.

Last week: 2 2.( Quick Gambling Yarn: Week after week, a gambler was losing his shirt on football. Each Saturday he’d bet on college games and each Sunday he’d bet on NFL games and each weekend he’d lose a bundle. He was the bookie’s dream. Then the Elite Youth Bobby Massie jersey football season neared an end, and the bookie was upset because of his anticipated loss of revenue. How, he wondered, could he keep this losing customer? Finally, he went to the guy and said, «Listen, hockey season is under way and we’ll be happy to take your action.» «Hockey,» said the man, insulted.