Study finds heart attack can trigger release of toxins that damage the brain

Recent research reveals that a heart attack can trigger the release of toxic substances in the body that have the potential to impair brain function and increase the risk of mental disorders, including cognitive decline. According to Neuroscience News on Friday, the study led by researchers from the University of Ottawa found that a molecule named methylglyoxal (MG) rises dramatically in the bloodstream after a heart attack and subsequently accumulates in the brain. The study was published in the journal Neuroscience: Advanced Science. Researchers explained that a heart attack places the body under severe stress, ranging from reduced oxygen, increased inflammation, to changes in metabolism. This condition triggers a spike in methylglyoxal, which then enters brain regions associated with emotion and cognitive function. Senior author Dr. Erik Suuronen said that methylglyoxal has previously been studied mainly in relation to metabolic diseases such as diabetes; however, the research team found that heart tissue damaged by a heart attack also produces the molecule in large amounts. “We predicted that methylglyoxal in the blood would target other organs including the brain, and that is what we found,” said Suuronen. The study also highlights high rates of depression and anxiety among heart attack patients. According to the researchers, heart attack patients have a risk of depression and anxiety up to three times higher than the general population. The researchers regard these findings as reinforcing the concept of the “heart-brain axis,” the bidirectional relationship between the heart and the brain. Inflammation and brain cell damage caused by methylglyoxal are also considered to potentially increase the risk of neurodegenerative diseases such as Alzheimer’s disease and dementia. The research team is now developing a peptide-based therapy designed to “capture” methylglyoxal before it harms brain cells. The therapy works like a molecular sponge that binds the toxin to prevent its entry into the central nervous system. Suuronen said the therapy will soon be tested to determine whether it can protect the brain of patients after a heart attack. If successful, the therapy could potentially help reduce the risk of mental disorders while also lowering the likelihood of a recurrent heart attack.