Chronic traumatic encephalopathy (CTE): criteria for neuropathological diagnosis and relationship to repetitive head impacts.

Autor: McKee AC; VA Boston Healthcare System, U.S. Department of Veteran Affairs, Boston, MA, USA. amckee@bu.edu.; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA. amckee@bu.edu.; Department of Neurology, Boston University School of Medicine, Boston, MA, USA. amckee@bu.edu.; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA. amckee@bu.edu.; VA Bedford Healthcare System, Bedford, MA, USA. amckee@bu.edu., Stein TD; VA Boston Healthcare System, U.S. Department of Veteran Affairs, Boston, MA, USA.; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA.; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.; VA Bedford Healthcare System, Bedford, MA, USA., Huber BR; VA Boston Healthcare System, U.S. Department of Veteran Affairs, Boston, MA, USA.; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA.; Department of Neurology, Boston University School of Medicine, Boston, MA, USA.; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA., Crary JF; Departments of Pathology, Neuroscience, and Artificial Intelligence and Human Health, Neuropathology Brain Bank and Research Core, Ronald M. Loeb Center for Alzheimer's Disease, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA., Bieniek K; Department of Pathology and Laboratory Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.; Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA., Dickson D; Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA., Alvarez VE; VA Boston Healthcare System, U.S. Department of Veteran Affairs, Boston, MA, USA.; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA.; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.; VA Bedford Healthcare System, Bedford, MA, USA., Cherry JD; VA Boston Healthcare System, U.S. Department of Veteran Affairs, Boston, MA, USA.; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA.; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA., Farrell K; Departments of Pathology, Neuroscience, and Artificial Intelligence and Human Health, Neuropathology Brain Bank and Research Core, Ronald M. Loeb Center for Alzheimer's Disease, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA., Butler M; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA., Uretsky M; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA., Abdolmohammadi B; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA., Alosco ML; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA.; Department of Neurology, Boston University School of Medicine, Boston, MA, USA., Tripodis Y; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA.; Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA.; Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA., Mez J; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA.; Department of Neurology, Boston University School of Medicine, Boston, MA, USA., Daneshvar DH; Boston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine, 150 S Huntington Ave, Boston, MA, 02130, USA.; Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA, USA.; Department of Physical Medicine and Rehabilitation, Massachusetts General Hospital, Boston, MA, USA.; Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Boston, MA, USA.
Jazyk: angličtina
Zdroj: Acta neuropathologica [Acta Neuropathol] 2023 Apr; Vol. 145 (4), pp. 371-394. Date of Electronic Publication: 2023 Feb 10.
DOI: 10.1007/s00401-023-02540-w
Abstrakt: Over the last 17 years, there has been a remarkable increase in scientific research concerning chronic traumatic encephalopathy (CTE). Since the publication of NINDS-NIBIB criteria for the neuropathological diagnosis of CTE in 2016, and diagnostic refinements in 2021, hundreds of contact sport athletes and others have been diagnosed at postmortem examination with CTE. CTE has been reported in amateur and professional athletes, including a bull rider, boxers, wrestlers, and American, Canadian, and Australian rules football, rugby union, rugby league, soccer, and ice hockey players. The pathology of CTE is unique, characterized by a pathognomonic lesion consisting of a perivascular accumulation of neuronal phosphorylated tau (p-tau) variably alongside astrocytic aggregates at the depths of the cortical sulci, and a distinctive molecular structural configuration of p-tau fibrils that is unlike the changes observed with aging, Alzheimer's disease, or any other tauopathy. Computational 3-D and finite element models predict the perivascular and sulcal location of p-tau pathology as these brain regions undergo the greatest mechanical deformation during head impact injury. Presently, CTE can be definitively diagnosed only by postmortem neuropathological examination; the corresponding clinical condition is known as traumatic encephalopathy syndrome (TES). Over 97% of CTE cases published have been reported in individuals with known exposure to repetitive head impacts (RHI), including concussions and nonconcussive impacts, most often experienced through participation in contact sports. While some suggest there is uncertainty whether a causal relationship exists between RHI and CTE, the preponderance of the evidence suggests a high likelihood of a causal relationship, a conclusion that is strengthened by the absence of any evidence for plausible alternative hypotheses. There is a robust dose-response relationship between CTE and years of American football play, a relationship that remains consistent even when rigorously accounting for selection bias. Furthermore, a recent study suggests that selection bias underestimates the observed risk. Here, we present the advances in the neuropathological diagnosis of CTE culminating with the development of the NINDS-NIBIB criteria, the multiple international studies that have used these criteria to report CTE in hundreds of contact sports players and others, and the evidence for a robust dose-response relationship between RHI and CTE.
(© 2023. The Author(s).)
Databáze: MEDLINE