Titre
Review: Contact sport-related chronic traumatic encephalopathy in the elderly: clinical expression and structural substrates.
Type
synthèse (review)
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Costanza, A.
Auteure/Auteur
Weber, K.
Auteure/Auteur
Gandy, S.
Auteure/Auteur
Bouras, C.
Auteure/Auteur
Hof, P.R.
Auteure/Auteur
Giannakopoulos, P.
Auteure/Auteur
Canuto, A.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1365-2990
Statut éditorial
Publié
Date de publication
2011
Volume
37
Numéro
6
Première page
570
Dernière page/numéro d’article
84
Peer-reviewed
Oui
Langue
anglais
Résumé
A. Costanza, K. Weber, S. Gandy, C. Bouras, P. R. Hof, P. Giannakopoulos and A. Canuto (2011) Neuropathology and Applied Neurobiology37, 570-584 Contact sport-related chronic traumatic encephalopathy in the elderly: clinical expression and structural substrates Professional boxers and other contact sport athletes are exposed to repetitive brain trauma that may affect motor functions, cognitive performance, emotional regulation and social awareness. The term of chronic traumatic encephalopathy (CTE) was recently introduced to regroup a wide spectrum of symptoms such as cerebellar, pyramidal and extrapyramidal syndromes, impairments in orientation, memory, language, attention, information processing and frontal executive functions, as well as personality changes and behavioural and psychiatric symptoms. Magnetic resonance imaging usually reveals hippocampal and vermis atrophy, a cavum septum pellucidum, signs of diffuse axonal injury, pituitary gland atrophy, dilated perivascular spaces and periventricular white matter disease. Given the partial overlapping of the clinical expression, epidemiology and pathogenesis of CTE and Alzheimer's disease (AD), as well as the close association between traumatic brain injuries (TBIs) and neurofibrillary tangle formation, a mixed pathology promoted by pathogenetic cascades resulting in either CTE or AD has been postulated. Molecular studies suggested that TBIs increase the neurotoxicity of the TAR DNA-binding protein 43 (TDP-43) that is a key pathological marker of ubiquitin-positive forms of frontotemporal dementia (FTLD-TDP) associated or not with motor neurone disease/amyotrophic lateral sclerosis (ALS). Similar patterns of immunoreactivity for TDP-43 in CTE, FTLD-TDP and ALS as well as epidemiological correlations support the presence of common pathogenetic mechanisms. The present review provides a critical update of the evolution of the concept of CTE with reference to its neuropathological definition together with an in-depth discussion of the differential diagnosis between this entity, AD and frontotemporal dementia.
PID Serval
serval:BIB_C93BC8D01A2B
PMID
Date de création
2011-09-29T07:30:05.082Z
Date de création dans IRIS
2025-05-20T23:50:16Z
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