A new study led by a team at the University of Ottawa takes a major step forward in understanding how heart attacks can dramatically alter brain function and cause neurological effects ranging from depression and anxiety to various types of cognitive decline.
This “heart-brain axis” concept suggests that neurological conditions after a heart attack may be caused in part by molecular changes caused by damage to the heart. Although many factors and signaling pathways are involved in the heart-brain interaction, this newly published study suggests that toxic byproducts produced within the body play a major role in the brain after a heart attack.
Brain inflammation after cardiac events
At the heart of this discovery is methylglyoxal (MG), a highly reactive molecule that surges into the bloodstream and accumulates in the brain after a heart attack. After a heart attack, the body enters a state of stress. Oxygen decreases, inflammation increases, and metabolism changes. As a result, MG levels in the bloodstream spike and accumulate in specific areas of the brain associated with mood and cognition.
The incidence of depression and anxiety in heart attack patients is up to three times higher than in the general population, and patients who suffer from depression and anxiety can be up to 2.7 times more likely to have another heart attack or die.
Delineating new areas in the connection between the brain and mind
The findings, published in the journal Advanced Sciences, could change recovery and long-term outcomes for millions of people as they reshape how scientists understand long-term risks after myocardial infarction and explain why emotional and cognitive impairments are so common after cardiac events.
Methylglyoxal has been widely studied for its role in metabolic diseases, including diabetes, but little is known about its function in other diseases. In previous research, we found that methylglyoxal is produced by heart tissue that dies after a heart attack (…) Based on this evidence, we predicted that methylglyoxal in the blood would target other organs and tissues, including the brain, and this is what we actually observed. ”
Dr. Eric Sulonen, senior author, full professor of surgery, faculty of medicine, scientist in the division of cardiac surgery, and director of the BeaTs research program at the University of Ottawa Heart Institute
Moving from discovery to treatment
The team’s findings raise important questions about neurodegenerative diseases, as chronic inflammation and cell damage in the brain are key factors in cognitive diseases such as dementia. By identifying methylglyoxal as a trigger, this study suggests a new pathway by which heart attacks may increase long-term neurological risks. Now that methylglyoxal has been identified as a potential target for the treatment of neurological disorders following a heart attack, the next step is to investigate how MG-induced inflammation causes neuronal death and mental health conditions.
Importantly, the research team has already developed a peptide therapeutic that can trap methylglyoxal and prevent it from damaging cells. “This treatment will soon be tested to see if it can protect the brain from damage after a heart attack,” Dr. Slonen says. If successful, they believe such treatments will do more than protect brain function. It may reduce your risk of future cardiac events.
“Given that heart attack patients who experience depression and anxiety have an increased risk of subsequent heart attack and death, reducing these symptoms could reduce subsequent serious cardiac events, improve the lives of countless patients, and meet an urgent unmet clinical need,” added Dr. Slonen.
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Reference magazines:
Forward, R.et al. (2026). Methylglyoxal accumulation is associated with post-myocardial infarction brain inflammation with gender and regional differences. cutting edge science. DOI: 10.1002/advs.202522584. https://advanced.onlinelibrary.wiley.com/doi/10.1002/advs.202522584?af=R
