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Summary: <\/strong>Researchers cracked a critical hidden mechanism behind the \u201cheart-brain axis,\u201d revealing how a heart attack physically reshapes brain function to cause depression, anxiety, and cognitive decline. The research demonstrates that following a cardiac event, a highly reactive, toxic byproduct called methylglyoxal (MG) surges into the bloodstream and aggregates inside mood and memory centers of the brain.<\/p>\n This discovery explains the biological link between cardiac stress and post-stroke psychiatric conditions while introducing an innovative peptide therapy designed to trap the toxin and shield vulnerable brain tissue.<\/p>\n Key Facts<\/strong><\/p>\n Source: <\/strong>University of Ottawa<\/p>\n A new study\u00a0led by a team from the University of Ottawa takes a major step forward in understanding how a heart attack can dramatically reshape brain function and trigger neurological effects, from depression and anxiety to different types of cognitive decline.<\/strong><\/p>\n This \u2018heart-brain axis\u2019 concept suggests that neurological conditions following a heart attack could be driven in part by molecular changes set in motion by damage to the heart. While there are many factors and signaling pathways involved in heart-brain interactions, this newly published research suggests that a toxic byproduct produced by the body plays a major role in the brain following a heart attack.<\/p>\n Brain inflammation after cardiac events<\/strong><\/p>\n At the center of the discovery is methylglyoxal (MG), a highly reactive molecule, which surges in the bloodstream and accumulates in the brain following a heart attack. Following a heart attack, the body enters a state of stress\u2014oxygen drops, inflammation rises, metabolism shifts\u2014causing MG levels to surge in the bloodstream and then accumulate in the brain in specific brain regions linked to mood and cognition.<\/p>\n The occurrence of depression and anxiety in heart attack patients is up to three times higher than the general population, with patients who suffer depression or anxiety may be up to 2.7 times more likely to experience another heart attack or death.<\/p>\n Charting new territory in brain-heart connection<\/strong><\/p>\n Published in the journal Advanced Sciences, this finding could potentially transform recovery and long-term outcomes for millions as it reshapes how scientists understand long-term risks after myocardial infarction and explain why emotional and cognitive disorders are so common after cardiac events. \u00a0<\/p>\n \u201cMethylglyoxal has been widely studied for its role in metabolic diseases, including diabetes, but much less is known about its function in other diseases. In a previous study, we discovered that methylglyoxal was produced by dying heart tissue after a heart attack (\u2026) based on this evidence, we predicted that methylglyoxal in the blood would target other organs and tissues, including the brain\u2014and this is what we did indeed observe,\u201d says senior author\u00a0Dr. Erik Suuronen, a Full Professor in the Faculty of Medicine\u2019s Department of Surgery, a scientist in the\u00a0Division of\u00a0Cardiac Surgery\u00a0and director of its\u00a0BEaTs Research Program\u00a0at the\u00a0University of Ottawa Heart Institute.<\/p>\n Moving from discovery toward therapy<\/strong><\/p>\n The team\u2019s discoveries raise important questions about neurodegenerative disease as chronic inflammation and cellular damage in the brain are key drivers of cognitive conditions like dementia.<\/p>\n By identifying methylglyoxal as a trigger, this research suggests a new pathway through which heart attacks could increase long-term neurological risk. Having identified methylglyoxal as a potential target for treating neurological disorders after a heart attack, the next step is to explore how MG-driven inflammation leads to neuron death and mental health conditions.<\/p>\n Importantly, the research team has already developed a peptide therapeutic that can trap methylglyoxal and prevent it from damaging cells.<\/p>\n \u201cThis therapy will soon be tested to see if it can protect the brain from damage after a heart attack,\u201d says Dr. Suuronen, who believes if successful, such treatments could do more than protect brain function; they could potentially reduce the risk of future cardiac events.<\/p>\n \u201cGiven the increased risk of subsequent heart attacks or death in heart attack patients who experience depression or anxiety, being able to alleviate these conditions could reduce subsequent major cardiac events and improve the lives of countless patients, filling an urgent unmet clinical need,\u201d Dr. Suuronen adds.<\/p>\n A<\/strong>: For decades, it was assumed to be purely psychological trauma, but this study proves a major physical, toxic link. When heart tissue dies during a heart attack, it pumps out a highly reactive, toxic byproduct called methylglyoxal (MG). This toxin travels through the bloodstream and pools inside the brain\u2019s emotional and memory centers, triggering cellular damage and inflammation that degrades brain health.<\/p>\n<\/div>\n A<\/strong>: The heart-brain axis is a two-way street. Once the toxic MG surge damages brain cells and triggers chronic mental health struggles, those psychiatric conditions feed straight back into your cardiovascular system. The persistent stress of anxiety and depression strains the heart, raising the likelihood of a secondary, fatal heart attack or death by 2.7 times.<\/p>\n<\/div>\n A<\/strong>: Think of it like a molecular sponge. The University of Ottawa team developed a custom peptide therapeutic specifically engineered to recognize, latch onto, and neutralize methylglyoxal in the body. By trapping this molecule before it can infiltrate the central nervous system, the drug prevents it from damaging brain tissue, shielding both your mental health and your long-term cognitive survival.<\/p>\n<\/div>\n<\/div>\n Author:\u00a0<\/strong>Paul Logothetis<\/a>\n
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About this neurology research news<\/h2>\n
Source:\u00a0<\/strong>University of Ottawa<\/a>
Contact:\u00a0<\/strong>Paul Logothetis \u2013 University of Ottawa
Image:\u00a0<\/strong>The image is credited to Neuroscience News<\/p>\n