Football Doesn’t Boost Alzheimer’s Protein, Study Finds

Research questions link between amateur play and brain disease risk

Contrary to recent fears, a new study suggests that amateur football may not elevate the risk of brain diseases like Alzheimer’s, offering a fresh perspective on the impact of contact sports.

Key Development

The Northwestern Medicine study, examining 174 donated brains, challenges the idea that amateur football increases specific proteins linked to Alzheimer’s and chronic traumatic encephalopathy (CTE). The research included brains from former high school and college football players.

“The long and short of it is no, this protein in this specific brain region is not increased in people who played football at the amateur level. It throws a little bit of cold water on the current CTE narrative.”

—Dr. Rudolph Castellani, corresponding author, professor of pathology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine neuropathologist

Published in the Journal of Alzheimer’s Disease, the study questions interpretations of subtle brain changes related to aging, Alzheimer’s, and repetitive head impacts. Consider that, according to the Alzheimer’s Association, in 2024, an estimated 6.9 million Americans age 65 and older are living with Alzheimer’s disease. (Alzheimer’s Association)

How the Study Worked

Scientists analyzed brain tissue from the Lieber Institute for Brain Development, focusing on men with psychiatric conditions, including 48 who played football. The study excluded professional athletes.

Researchers examined the CA2 region of the hippocampus, a memory-related area. Phosphorylated tau (p-tau) protein, often found in neurodegenerative diseases, accumulates here. However, the study indicates that p-tau buildup in CA2 isn’t tied to contact sports. Its presence correlated with age, not football participation.

“What’s novel here is a return to the null hypothesis – that there may be no link between repeated head injuries and p-tau buildup in this location,” said Castellani, also neuropathology core director of the Northwestern University Alzheimer’s Disease Research Center. “Rather than assuming p-tau in CA2 is inherently pathological, we’re asking whether it might be part of normal aging or a non-specific response to environmental factors.”

The study highlights challenges in neurodegeneration research, especially assigning clinical meaning to subtle pathological findings. The authors emphasize difficulties in defining CTE in clinically meaningful terms.

“Modern studies on CTE may be expanding the boundaries of what’s considered normal variability in the human brain,” Castellani said. “This work reminds us to be cautious in interpreting pathology without clear clinical correlation.”

Larger studies are needed to clarify how p-tau relates to aging and head injuries, prompting a critical evaluation of what defines neurodegenerative disease.