Dementia Pugilistica with clinical features of Alzheimer's disease

Areza-Fegyveres, Renata; Rosemberg, Sérgio; Castro, Rosa Maria R.P.S.; Porto, Cláudia Sellitto; Bahia, Valéria Santoro; Caramelli, Paulo; Nitrini, Ricardo

doi:10.1590/s0004-282x2007000500019

Cited by 38 publications

(28 citation statements)

References 9 publications

(12 reference statements)

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“…In addition, the progressive memory impairment observed in more than 80% of our CTE cases, and in all 10 of the subjects with dementia, could lead to an inaccurate diagnosis of AD when the underlying disease is CTE. 12 It is not clear what neuropathologic changes may lead to the 2 possible clinical presentations observed in this study. It is unlikely that the small, focal cortical p-tau lesions found in stage I and II CTE produce clinically meaningful behavioral and mood symptoms.…”

Section: Resultsmentioning

confidence: 85%

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Clinical presentation of chronic traumatic encephalopathy

Daneshvar²,

et al. 2013

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Objective: The goal of this study was to examine the clinical presentation of chronic traumatic encephalopathy (CTE) in neuropathologically confirmed cases.Methods: Thirty-six adult male subjects were selected from all cases of neuropathologically confirmed CTE at the Boston University Center for the Study of Traumatic Encephalopathy brain bank. Subjects were all athletes, had no comorbid neurodegenerative or motor neuron disease, and had next-of-kin informants to provide retrospective reports of the subjects' histories and clinical presentations. These interviews were conducted blind to the subjects' neuropathologic findings.Results: A triad of cognitive, behavioral, and mood impairments was common overall, with cognitive deficits reported for almost all subjects. Three subjects were asymptomatic at the time of death. Consistent with earlier case reports of boxers, 2 relatively distinct clinical presentations emerged, with one group whose initial features developed at a younger age and involved behavioral and/or mood disturbance (n 5 22), and another group whose initial presentation developed at an older age and involved cognitive impairment (n 5 11). Conclusions:

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Section: Resultsmentioning

confidence: 85%

“…[11][12][13] Herein, we describe the clinical presentation, course, and APOE genotype of a sample of 36 athletes with neuropathologically confirmed CTE.…”

mentioning

confidence: 99%

Clinical presentation of chronic traumatic encephalopathy

Daneshvar²,

et al. 2013

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“…Thus, the original hallmark of dementia pugilistica-neurofibrillary degeneration without plaques-is now amended to include diffuse plaques in a significant subset of cases. 64,67,68 Dementia pugilistica in its pure form is still said to lack the neuritic plaques more characteristic of AD, but the presence of diffuse Ab deposits along with studies showing increased Ab in the acute state after trauma, 69 has led some investigators to propose a role of the amyloid cascade in chronic sequelae of head trauma, 70 not unlike the proposed role for Ab precursor protein (AbPP) in AD pathogenesis.…”

Section: Amyloid Betamentioning

confidence: 99%

Neurodegeneration and Sport

Castellani

McCrory

2015

Neurosurgery

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The recent interest in concussion in sport has resulted in significant media focus about chronic traumatic encephalopathy (CTE), although a direct causative link(s) between concussion and CTE is not established. Typically, sport-related CTE occurs in a retired athlete with or without a history of concussion(s) who presents with a constellation of cognitive, mood, and/or behavioral symptoms and who has postmortem findings of tau deposition within the brain. There are many confounding variables, however, that can account for brain tau deposition, including genetic mutations, drugs, normal aging, environmental factors, postmortem brain processing, and toxins. To understand the roles of such factors in neurodegenerative diseases that may occur in athletes, this article reviews some neurodegenerative diseases that may present with similar findings in nonathletes. The article also reviews pathological changes identified with normal aging, and reviews the pathological findings of CTE in light of all these factors. While many of these athletes have a history of exposure to head impacts as a part of contact sport, there is insufficient evidence to establish causation between sports concussion and CTE. It is likely that many of the cases with neuropathological findings represent the normal aging process, the effects of opiate abuse, or a variant of frontotemporal lobar degeneration. Whether particular genetic causes may place athletes at greater risk of neurodegenerative disease is yet to be determined.

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“…Of the 10 subjects diagnosed with dementia before death (four with clinical AD, four with 'dementia pugilistica' or 'footballrelated' dementia and two with unspecified dementia), all were diagnosed with stage IV CTE after post-mortem examination. This suggests that the overlap of clinical symptoms between CTE and AD, such as progressive memory impairment, could lead to an incorrect diagnosis of AD instead of CTE during life [1,13,63].…”

Section: Clinical Sub-typesmentioning

confidence: 99%