Medical Bulletin 11/ December/ 2024

The short-term boost our brains get after we do exercise persists throughout the following day, suggests a new study led by UCL researchers. The new study, published in the International Journal of Behavioral Nutrition and Physical Activity, found that, on average, people aged 50 to 83 who did more moderate to vigorous physical activity than usual on a given day did better in memory tests the day after.

Less time spent sitting and six hours or more of sleep were also linked to better scores in memory tests the next day. More deep sleep also contributed to memory function, and the research team found this accounted for a small portion of the link between exercise and better next-day memory.

The research team looked at data from 76 men and women who wore activity trackers for eight days and took cognitive tests each day. In the short term, exercise increases

blood flow to the brain and stimulates the release of neurotransmitters such as norepinephrine and dopamine which help a range of cognitive functions. These neurochemical changes are understood to last up to a few hours after exercise. However, the researchers noted that other brain states linked to exercise were more long-lasting. For instance, evidence suggests exercise can enhance mood for up to 24 hours.

For the new study, the researchers looked at data from wrist-worn activity trackers to determine how much time participants spent being sedentary, doing light physical activity, and doing moderate or vigorous physical activity. They also quantified sleep duration and time spent in lighter sleep and deeper, slow-wave sleep.

They also accounted for participants’ average levels of activity and sleep quality across the eight days they were tracked, as participants who are habitually more active and typically have higher-quality sleep perform better in cognitive tests.

The team found that more moderate or vigorous physical activity compared to a person’s average was linked to better working memory and episodic memory the next day. More sleep overall was linked to improved episodic and working memory and psychomotor speed. More slow-wave sleep was linked to better episodic memory. Conversely, more time spent being sedentary than usual was linked to worse working memory the next day.

New research from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London provides valuable insights into the brain-body immune connection identifying key communication hubs in the dural sinuses and skull bone marrow at the back of the head.

The research that was published in the journal Brain, used neuroimaging techniques to establish that the dural sinuses, a region at the back of the head that drains deoxygenated blood from the brain, as well as the skull bone marrow act as a likely interface between the central and peripheral immune systems.

Researchers analysed a dataset of 51 adults with depression, as well as 25 healthy age matched participants that were originally recruited as part of the BIODEP study to investigate the role of inflammatory processes in depression. Each subject provided a blood sample before undergoing a PET scan and MRI during the original data collection. Peripheral inflammatory markers were assessed from blood while inflammatory activity in the anterior cingulate cortex, skull marrow, and dural sinuses was assessed with PET sensitive to immune cell density.

An analysis of the data revealed that the inflammatory activity in dural sinuses and skull marrow, which the researchers identified as a potential reservoir of immune cells, is closely associated with inflammatory activity in both the body and the brain, and this association was present in those with depression and in healthy controls. This association was stronger in the dural sinuses than in the skull marrow.

Brandi Eiff, the study’s first author from King’s IoPPN said, “There are many conditions for which inflammation is a factor. By establishing this link, we can better understand how peripheral immunity interacts with brain function and mental health. As science and medicine begins to move toward a more holistic approach, considering the immune responses across the brain and body could be valuable in terms of advancing treatments of many disorders, including depression.”

Reference: Eiff, B., Bullmore, E. T., Clatworthy, M. R., Fryer, T. D., Pariante, C. M., Mondelli, V., ... & Schubert, J. J. (2024). Extra-axial inflammatory signnal and its relation to peripheral and central immunity in depression. medRxiv, 2024-03.

Researchers at Karolinska Institutet and the University of Gothenburg have identified two types of metabolic-associated

fatty liver disease – a liver-specific type and a systemic type that affects other organs and tissues. The discovery could lead to improved diagnosis and treatment of this growing patient group. Two studies are published back-to-back in Nature Medicine.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterised by an excessive accumulation of fat in the liver, which can lead to severe liver damage such as cirrhosis and

liver cancer. Metabolic dysfunction-associated steatotic liver disease is caused by overweight and obesity and it is a major and growing burden globally.

“We discovered that there are at least two types of steatotic liver disease with different clinical trajectories,” says Stefano Romeo, Professor at the Department of Medicine, Huddinge, Karolinska Institutet, who led the research. “One is more aggressive and mainly affects the liver, while the other is entwined in the cardio-renal-metabolic syndrome.”

The researchers used genetic tests to identify 27 new genetic variants linked to Metabolic dysfunction-associated steatotic liver disease. By analysing these genes, they were able to determine two different risk scores related to the two types of Metabolic dysfunction-associated steatotic liver disease. The liver-specific type is more aggressive and can lead to severe liver damage but protects against cardiovascular disease, while the systemic type is associated with a higher risk of diabetes, cardiovascular disease, heart and kidney failure.

The study also highlights the importance of genetic research in understanding complex diseases like Metabolic dysfunction-associated steatotic liver disease and the mechanisms causing the cardio-renal-metabolic syndrome.

Reference: Jamialahmadi, O., De Vincentis, A., Tavaglione, F. et al. Partitioned polygenic risk scores identify distinct types of metabolic dysfunction-associated steatotic liver disease. Nat Med (2024). https://doi.org/10.1038/s41591-024-03284-0

Researchers at Lund University Diabetes Centre, have led a study that has mapped out differences in the atherosclerotic process in people who have type 2 diabetes and in people who do not have the disease. The study has now been published in Nature Communications.

"A stroke or heart attack often leads to reduced quality of life and, in the worst-case scenario, death. Since we know that people with type 2 diabetes have a higher risk of being affected, we set particularly ambitious treatment goals for patients with atherosclerosis and type 2 diabetes. Current treatment options mainly target risk factors such as blood lipids, blood pressure and lifestyle, regardless of whether the person has diabetes or not. Our new study provides additional evidence that people with type 2 diabetes may need new treatments that target specific molecular mechanisms of atherosclerosis," says Andreas Edsfeldt, cardiologist and associate professor at Lund University Diabetes Centre.

The researchers have carried out detailed analyses of atherosclerotic plaques from a total of 219 individuals with cardiovascular diseases, and of these, 72 had type 2 diabetes. Atherosclerosis means that fats, cells, calcium and connective tissue have accumulated for a long time on the inside of the arteries, forming what are known as atherosclerotic plaques. The research team found that atherosclerotic plaques from patients with type 2 diabetes had lower levels of protective connective tissue in comparison with plaques from those without diabetes. The reason for this seems to be a lack of a specific growth factor called TGF-beta2. The research team also found that high blood sugar levels can be linked to a reduced ability to form protective connective tissue in the atherosclerotic plaques, which leads to an increased risk of stroke or heart attack.

Reference: Singh, P., Sun, J., Cavalera, M. et al. Dysregulation of MMP2-dependent TGF-ß2 activation impairs fibrous cap formation in type 2 diabetes-associated atherosclerosis. Nat Commun 15, 10464 (2024). https://doi.org/10.1038/s41467-024-50753-8