Saed News: A heart attack can significantly alter brain function and cause neurological effects such as depression, anxiety, and various forms of cognitive decline.
According to SAEDNEWS, the concept of the “heart–brain axis” suggests that neurological conditions after a heart attack may partly result from molecular changes that occur following damage to the heart. Although multiple factors and signaling pathways are involved in the connection between the heart and brain, current research indicates that a toxic byproduct produced by the body plays a key role in the brain after a heart attack.
At the center of this discovery is methylglyoxal (MG), a highly reactive molecule whose levels increase in the bloodstream after a heart attack and accumulate in the brain. After a heart attack, the body enters a state of stress (reduced oxygen, increased inflammation, and metabolic changes), which leads to a surge of methylglyoxal in the blood and its accumulation in specific brain regions related to mood and cognition.
The prevalence of depression and anxiety in heart attack patients is up to three times higher than in the general population. In addition, patients who suffer from depression or anxiety are up to 2.7 times more likely to experience another heart attack or death.
This finding could transform recovery processes and long-term outcomes for millions of people, as it changes scientists’ understanding of long-term risks after a heart attack and explains why emotional and cognitive disorders are so common after cardiac events.
Eric Soronen, the lead researcher of this study and professor in the Department of Surgery at the University of Ottawa Medical School in Canada, stated: Methylglyoxal has mostly been studied in metabolic diseases such as diabetes, but its role in other diseases was less known. In previous research, we found that methylglyoxal is produced by dying heart tissue 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 exactly what we observed.
The findings of this research group raise important questions about neurodegenerative diseases, as chronic inflammation and cellular damage in the brain are key drivers of conditions such as dementia. By identifying methylglyoxal as a triggering factor, this study presents a new pathway through which a heart attack can increase long-term neurological risks. After identifying methylglyoxal as a potential target for treating post-heart-attack neurological disorders, the next step is to investigate how inflammation caused by methylglyoxal leads to neuron death and the development of mental illnesses.
According to Medical News, more importantly, the research team has already developed a peptide drug that can trap methylglyoxal and prevent it from damaging cells.
Soronen says: This treatment will soon be tested to determine whether it can protect the brain from damage after a heart attack. He believes that if successful, such treatments would go beyond protecting brain function and could potentially reduce the risk of future cardiac events.
He added: Given the increased risk of recurrent heart attacks or death in patients who develop depression or anxiety after a heart attack, the ability to reduce these conditions could lower major subsequent cardiac risks, improve the lives of countless patients, and address an urgent and unmet clinical need.
