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Longevity Briefs: How The Brain Could Be Playing An Important Role In Heart Disease

Posted on 24 May 2022

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Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

Why is this research important: Atherosclerosis is a disease in which white blood cells called monocytes attack cholesterol that has become trapped in the walls of arteries. These white cells become trapped too, die, and eventually form fatty plaques that can obstruct blood flow or rupture and cause blood clots. The plaque itself is not connected to the central nervous system, but the outer layer of the artery is, and white cells collect there in atherosclerosis. Could atherosclerosis have an effect on the central nervous system?

What did the researchers do: In this study published in the journal Nature, researchers studied aortas of mice that are genetically predisposed to develop atherosclerosis (Apoe−/− mice) as well as aorta samples removed from human patients as part of surgery. These and other tissues such as lymph nodes and spleen tissue were studied using a variety of techniques including staining using fluorescently tagged antibodies and measurements of gene expression.

Key takeaway(s) from this research: Researchers found, for the first time, evidence of a ‘nervous circuit’ in which the central nervous system promotes the progression of atherosclerosis. They found that in atherosclerosis in both humans and mice, white blood cells gather in the outer layer of the diseased blood vessel to form a structure similar to a lymph node, with a rich concentration of nerve fibres. At least in mice, these nerve fibres send signals to the brain, which in turn sends signals to the spleen. The spleen contains a reserve of white cells (monocytes) which become activated by this signal, entering the circulation where they can find the fatty plaque and further contribute to its growth.

The activity of this ‘artery-brain circuit’ was enhanced during ageing, but the researchers also found that when nervous connections to the spleen were disrupted in live mice using a neurotoxic drug, the mice’s fatty plaques stopped growing and stabilised.

More research will be needed to confirm these findings and explore them in more detail. If this disease mechanism is similarly important in humans, it could provide valuable targets for treating atherosclerosis.

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