A recent international, multi-centre study published in JAMA Neurology, coordinated by researchers from UHN’s Krembil Brain Institute (KBI), revealed that repeated head impacts (RHI) have more far-reaching effects that previously thought.
The last few years have seen a resurgence of discourse on the long-term effects of RHI, particularly for professional athletes such as football players and boxers. RHI is associated with an increased risk of chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease that can cause behavioural issues and cognitive decline.
CTE can only be diagnosed by examining the brain for CTE neuropathological change (CTE-NC) after an individual dies. CTE-NC is characterized by abnormal accumulations, called aggregates, of a misshapen form of the tau protein in neurons and astrocytes—cells that support neurons—in their brain’s cortex. However, until now, research has focused almost exclusively on the brain, overlooking another vulnerable part of the nervous system: the spinal cord.
Dr. Gabor Kovacs, a Senior Scientist at KBI, and his research team set out to address this gap by examining the effects of RHI on the spinal cord. In this postmortem study, the team analyzed brain and spinal cord tissue from 70 individuals for the presence and severity of CTE-related tau aggregates beyond the brain.
They found that individuals with CTE-NC in the brain showed significantly more frequent and severe tau aggregates in the spinal cord than those without CTE, regardless of RHI history. Notably, CTE cases also exhibited tau aggregates in spinal astrocytes, which is a feature not seen in other conditions with tau aggregates such as Alzheimer disease.
Among those with CTE, both neuronal and astrocytic tau pathology were more pronounced in individuals with a history of RHI, highlighting a cumulative effect of repeated trauma.
Age further amplified these changes with individuals over the age of 65 who had a both CTE and a history of RHI exhibiting the most severe tau aggregates. Other protein aggregates in the brain were also seen in the spinal cord, including α-synuclein, amyloid-beta, and TDP-43, which contribute to Parkinson disease, Alzheimer disease, and amyotrophic lateral sclerosis, respectively. These other protein aggregates were also more common in this group—suggesting that RHI may accelerate age-related neurodegeneration and contribute to the development of other conditions beyond CTE.
“For too long, the effects of repeated impacts on the central nervous system beyond the brain have been understudied,” says first author Dr. Hidetomo Tanaka. Dr. Kovacs adds, “It is time we shift the definition of CTE to encompass not only the brain but the spinal cord as well.”
By broadening the scope of CTE research, this work deepens our understanding of trauma-related neurodegeneration and underscores the need for protective strategies to safeguard the spine as well as the brain for those at risk of RHI. Ultimately, these insights may help reduce long-term neurological burden later in life and improve quality of life for those impacted by RHI—including former professional athletes long after their sport careers have ended.
The first author of this study is Dr. Hidetomo Tanaka, a neuropathologist and a Research Fellow at the Tanz Centre for Research in Neurodegenerative Disease (CNRD) at the University of Toronto.
The senior author of this study is Dr. Gabor G. Kovacs, a Senior Scientist at UHN’s Krembil Brain Institute (KBI), a Professor in the Department of Laboratory Medicine and Pathobiology at the University of Toronto, and a Principal Investigator at the Tanz CRND at the University of Toronto.
Drs. Carmela Tartaglia, a Clinician Investigator at KBI, and Charles Tator, a Senior Scientist at KBI, are co-authors of this study.
This work was supported by the National Institutes of Health (NIH), the United States Department of Defense, the Medical Research Council, and UHN Foundation.
Dr. Kovacs has a shared patent for 5G4 synuclein and a patent pending for diagnostic assays for movement disorders. He also reported royalties from Wiley, Cambridge, Taylor and Francis, as well as research support from the Rossy Family Foundation, Edmond Safra Foundation, Krembil Foundation, MSA Coalition, Michael J. Fox Foundation, Parkinson Canada, and the NIH outside of this work.
For a complete list of other authors’ conflicts, see the publication.
Tanaka H, Black LE, Forrest SL, Danics K, Sadia N, Khodadadi M, Tator C, Smith DH, Tartaglia MC, Stewart W, Kovacs GG. Spinal Cord Tau and Protein Copathologies Associated with Chronic Traumatic Encephalopathy. JAMA Neurol. 2026 Jan 26. DOI: 10.1001/jamaneurol.2025.5421.