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An analysis of sex differences in the genetics of schizophrenia, bipolar disorder and major depressive disorders indicates that while there is substantial genetic overlap between males and females, there are noticeable sex-dependent differences in how genes related to the central nervous system, immune system, and blood vessels affect people with these disorders.
The findings, from a multinational consortium of psychiatric researchers including investigators and a senior author at Massachusetts General Hospital (MGH), could spur better treatments for major psychiatric disorders. They are published in the journal Biological Psychiatry.
The findings were made possible only through the cooperation of more than 100 investigators and research groups, who combed through the genomes of 33,403 people with schizophrenia, 19,924 with bipolar disorder, and 32,408 with major depressive disorder, as well as 109,946 controls (people without any of these diagnoses).
Their goal was to understand why these major psychiatric disorders differed between the sexes. For example, women have a significantly higher risk for major depressive disorder, whereas the risk for schizophrenia is significantly higher among men. The risk of bipolar disorder is about the same for both women and men, but disease onset, course, and prognosis differ markedly between the two.
“We’re in the era of Big Data, and we’re looking for genes that are associated with illnesses to identify druggable targets associated with the genotype, in order to develop more effective treatments for that illness that may differ by sex,” says senior author Jill M. Goldstein, PhD, founder and executive director of the Innovation Center on Sex Differences in Medicine (ICON) at MGH.
Goldstein and colleagues searched for clues in the form of single nucleotide polymorphisms, or SNPs (“snips”), in which a single DNA “letter” (nucleotide) differs from one person to the next and between sexes.
“There are sex differences in the frequency of chronic diseases and cancers as well. It’s pervasive,” says Goldstein, who is also a professor of Psychiatry and Medicine at Harvard Medical School. “But medicine, essentially, has been built on models of men’s health and male animals. We need to develop our precision medicine models incorporating the effect of sex.”
By taking advantage of large psychiatric databases, the investigators were able to demonstrate that the risks for schizophrenia, bipolar disorder and major depressive disorder are affected by interactions of specific genes with sex, apart from the effects of sex hormones such as estradiol or testosterone.
For example, the investigators found interactions with schizophrenia and depression and sex in genes controlling for the production of vascular endothelial growth factor, a protein that promotes the growth of new blood vessels.
“My lab is studying the substantial co-occurrence of depression and cardiovascular disease. It turns out that both depression and schizophrenia have a very high co-occurrence with cardiovascular disease. We believe there are shared causes between psychiatric and cardiovascular diseases that are not due to the effects of medication,” she says. “In addition, the co-occurrence of depression and cardiovascular disease is twice as high in women as in men, and this may, in part, be associated with our finding in depression of sex differences in a gene controlling vascular endothelial growth factor.”
The investigators emphasize that although the specific causes of the diseases they studied are still unknown, “our study underscores the importance of designing large-scale genetic studies that have the statistical power to test for interactions with sex. Dissecting the impact of sex, genes, and pathophysiology will identify potential targets for sex-dependent or sex-specific therapeutic interventions creating more effective therapies for both men and women,” she says.
The analyses were supported by private donor Gwill York, the National Institute of Mental Health and the NIH Office for Research on Women’s Health.

A new technique that can trace which tissues and organs the DNA in our blood comes from has been reported today in the open-access eLife journal.
The method, called GETMap, could be used in prenatal screening, to monitor organ transplant rejection, or test for cancers that are concealed in the body.
“Analysis of circulating free DNA has been shown to be useful for screening for early asymptomatic cancers,” explains first author Wanxia Gai, Postdoctoral Fellow at the Chinese University of Hong Kong, Hong Kong SAR, China. “As cancer-associated DNA changes are present in a wide range of cancer types, detection of such changes can be used as a universal test for concealed cancers. However, in patients with a positive test result, you still need to follow up with tests to find the tumour’s location, for example, with a whole-body positron emission tomography, or PET, scan.”
To address this, the team developed a test that looks for genetic differences, as well as epigenetic changes to DNA (changes which do not affect DNA sequences) known as methylation. The DNA in our cells has a unique methylation ‘fingerprint’. Comparing the methylation fingerprints of different genetic types of DNA molecules circulating in the blood, for example molecules from a fetus, transplanted organ or tumour, with that of different tissues identifies where the DNA has come from.
The team first tested their approach in pregnant women, where they knew that blood DNA would include DNA from the mother, fetus, or both. As expected, GETMap found that DNA carrying fetus-specific genetic markers carried methylation signatures exclusively from the placenta. On the other hand, DNA molecules carrying mother-specific genetic markers carried methylation signatures from white blood cells. DNA molecules carrying genetic markers shared by both the mother and fetus were derived from both tissues.
Next, they tested the approach in blood donated by patients following a lung transplant. Detecting unusually high concentrations of DNA from a transplanted organ in blood can be a sign of organ rejection. But immediately after a transplant, there is often an unexplained surge in donor-derived DNA in the transplant recipient’s blood. This makes it challenging to detect whether the organ is being rejected if only genetic markers are used. By using a combination of genetic and epigenetic markers, the team identified the origins of this surge in donor DNA. At 72 hours after transplantation, only 17% of the circulating DNA was from the lung, compared with 78% from blood cells. This surprisingly high contribution from the blood cells was likely due to the release of DNA from blood cells in the blood vessels of the transplanted lung. With time, the amount of circulating DNA from the lung increased, and the amount from blood cells decreased. There also seemed to be more donor lung DNA in the blood of patients whose new lungs were rejected, compared to those who had a successful transplant.
The team also tested whether GETMap could detect the origin of tumour-derived DNA in the blood. In two patients with liver cancer, they found that 90% and 87% of the plasma DNA carrying mutations had come from the liver. To test this, they needed to know the exact tumour mutations they were looking for, and tumour tissue is not always available if its location is unknown. The team therefore tried to use methylation fingerprints to identify cancer mutations directly from blood DNA rather than tumour tissue. Although fewer mutations were found, the liver was still correctly identified as the source of the tumour-derived molecules. This suggests GETMap could help to reveal the tissue and location of concealed cancers in people who have tumour markers in their blood.
Finally, they challenged the GETMap test in a woman who developed lymphoma during pregnancy. In this instance, they were able to distinguish between the fetal-specific genes which were derived from the placenta, and the tumour-specific genes which originated solely from a family of white blood cells that were related to the cell type of the lymphoma.
“We have demonstrated the powerful synergy between genetic and epigenetic approaches for identifying the origin of circulating DNA in the blood, and shown its potential applications in cancer screening, prenatal testing and organ transplant monitoring,” says co-senior author Dennis Lo, Director of the Li Ka Shing Institute of Health Sciences, and the Li Ka Shing Professor of Medicine at the Chinese University of Hong Kong.
“Our test could bring us closer to the vision of a blood test for a universal cancer marker, by allowing more targeted follow-up tests in specific organs,” concludes co-senior author Allen Chan, Professor of Chemical Pathology at the Chinese University of Hong Kong. “This could make cancer diagnosis earlier and more accurate, and reduce the use of whole-body scans and the associated exposure to radiation.”
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Materials provided by eLife. Note: Content may be edited for style and length.

SharecloseShare pageCopy linkAbout sharingimage copyrightReutersThe Duke of Sussex is to become chief impact officer at the US coaching and mental health firm, BetterUp.Prince Harry said in a statement that he was “really excited” about taking on the new role. His exact duties, hours and any payment are not clear.It is his latest job move after he and the Duchess of Sussex stepped back as senior royals in March last year.It also comes after the duke and Meghan gave an explosive interview to Oprah Winfrey earlier this month.In it, the couple alleged an unnamed royal family member had asked about how dark their son Archie’s skin might be, before he was born.Buckingham Palace has said the claim is “concerning”, but it will be addressed privately. Earlier this week, Buckingham Palace said a diversity review was under way across all royal households.12 things we learned from Meghan’s Oprah interviewHarry and Meghan step backHarry and Meghan rattle monarchy’s gilded cageIn his statement, Prince Harry said his goal in his new function would be to “lift up critical dialogues around mental health, build supportive and compassionate communities, and foster an environment for honest and vulnerable conversations”.Prince Harry will not manage employees or have people report directly to him, but he is likely to spend some time in the company’s San Francisco headquarters once it is safe to do so, BetterUp CEO Alexi Robichaux told the Wall Street Journal (WSJ). In his role as the company’s first chief impact officer, Prince Harry is expected to have input into initiatives including product strategy decisions and charitable contributions, and advocate publicly on topics related to mental health, the WSJ reports.Prince Harry said that when he met Mr Robichaux, they “instantly recognised a shared passion for helping others realise their full potential”.The chief impact officer position is relatively rare in the corporate world, notes the WSJ – it is seen more commonly in non-profit organisations such as Amnesty International.BetterUp, which was founded in 2013, provides mobile-based professional coaching, counselling and mentorship.The firm says it has some 2,000 coaches offering services in 49 languages in 66 countries.Prince Harry has previously launched initiatives such as the Invictus Games, which aim for members of the armed forces to use sport for psychological and physical rehabilitation. He has also advocated publicly on mental health issues.Prince Harry and Meghan now live in California after confirming in January that they would step back as “senior” royals and work to become financially independent.They announced last year that they had reached a deal with streaming giant Netflix to make a range of programmes, some of which they may appear in, as well as striking a deal with music streaming service Spotify.Where do Harry and Meghan get their money?

SharecloseShare pageCopy linkAbout sharingimage copyrightEPAVladimir Putin has been vaccinated against Covid-19, partly to encourage other Russians who remain deeply reluctant to get the jab.Although he has previously been filmed on horseback, ice skating and flying with Siberian cranes, he chose to be vaccinated behind closed doors.The Kremlin has not specified which vaccine Mr Putin received.The aim was to underline “all three Russian vaccines are absolutely reliable, very good and effective,” spokesman Dmitry Peskov said. Speaking to the BBC, he brushed off the suggestion that showing President Putin getting a shot in the arm would help persuade the sceptical majority of Russians to follow suit. As for believing the president actually had the jab, he said people would just have to “take our word for it”.There’s likely to be a limited increase in the slow pace of vaccination as a result.Grand plans, low interestThe president’s own daughter took part in the Sputnik V safety trials, but he’s seemed oddly cautious given how highly he recommends the jab for others. Mr Putin, who is 68 years old, initially claimed he was waiting until it had been deemed safe for the over-65s. Later he said he’d wait for autumn when his doctors could fit the Covid shot in his “vaccine schedule”. Mr Putin also told a gathering of Russian news editors that he wouldn’t be a “performing monkey” and get vaccinated before the TV cameras, surprising many with his sudden camera-shyness. Mr Putin revealed on Monday that 6.3 million Russians had so far received one dose of a Covid vaccine since he became the world’s first leader to announce a “large-scale” vaccination back in December. That’s only around 5% of the adult population.image copyrightReutersHis target is to protect 60% of adults by July – sufficient for “collective immunity” to stop the virus spreading. But that would require boosting the current vaccination-rate from just a few thousand to more than 700,000 every day – and that’s just a single dose of the vaccine.Despite Russia touting its most widely available jab, Sputnik V, as the world’s first and best, interest at home is low and falling. Why many in Russia are reluctant to have Sputnik vaccineA Levada-Center poll suggests the number of Russian opposed to getting it rose to 62% in February, with most citing concerns over possible side effects despite the fact Sputnik proved safe and almost 92% effective in trials. Many also see no urgent need for protection. There’s been no lockdown here since spring 2020, the number of new infections is currently falling and the death toll from Covid is barely mentioned. The daily count has reached 95,818, though the number of excess deaths recorded so far is some four times higher.Read more from Sarah here: How Russia glosses over its Covid death tollGlobal ambition Meanwhile, enthusiasm for Russia’s main vaccine has been increasing abroad.On Tuesday, Vietnam became the 56th country to register Sputnik and Russia says it has done deals to supply 700 million doses of the vaccine overseas.But it’s unclear when that demand can be met. Russia plans to transfer the technology for production abroad but Sputnik’s backer, the Russian Direct Investment Fund, will not answer questions about any current supply from overseas facilities or its targets.In a call with scientists and producers on Monday, President Putin was full of praise for their achievements with three Russian vaccines now registered for emergency use, including EpiVacCorona and CoviVac.A batch of a new version of Sputnik V that doesn’t need freezing has just been distributed and trials on the one-jab Sputnik Light have concluded. But scaling up production has proved complicated. Total vaccine output will increase to 12.5 million “units” of two doses in March, according to the industry ministry, with an extra five million units added in April. Still, there have been reports of shortages in some Russian regions.One clinic the BBC visited this month in Perm admitted it had run out of the first dose of Sputnik and didn’t expect more for several days. Putin back to business Now he’s been vaccinated, it’s possible Russians could be seeing more of Mr Putin in the flesh.He has spent much of the pandemic working from his official residence outside Moscow. Those meeting him in person have had to quarantine first. The Kremlin says he is getting vaccinated now in order to have the “necessary level of immunity” to get back to travelling and working, ahead of parliament elections in autumn.You may also be interested in:

Cold Spring Harbor Laboratory (CSHL) President and CEO Bruce Stillman has been dissecting DNA replication, a critical step in cell division, since the 1980s. His lab studies how Origin Recognition Complexes — ORCs — coordinate DNA duplication. They discovered how our cells assemble and disassemble ORCs during the cell division cycle. One ORC protein is sequestered into small liquid droplets, keeping it apart until the right time to recruit other proteins and initiate DNA replication.
The ORC recognizes where to initiate replication at numerous locations along the long, linear stretches of DNA in our cells’ chromosomes. Fully assembled ORCs recruit other proteins to make precise copies of the chromosomes. This mechanism is necessary to inherit DNA accurately without errors that can lead to disorders such as cancer.
Scientists have studied the structure of ORCs in several species. Stillman explains:
“We’ve previously studied this in baker’s yeast, but it turns out that human cells have a different way of doing things.”
Unlike single-celled yeast, humans have a variety of cells that divide at different times. To choreograph this, the researchers found that one human ORC protein, ORC1, has certain regions that yeast ORC1 lacks. When ORC binds to DNA, ORC1 recruits CDC6, a protein that assembles other DNA replication proteins. Some of the human-specific regions of ORC1 and CDC6 bind other proteins that regulate DNA replication. Manzar Hossain, a research investigator in Stillman’s lab, says:
“We found that ORC1 and CDC6 interact in a very tangential manner. We found a very short time period which allows them to interact.”
DNA-bound ORC1 is sequestered into liquid droplets that briefly change shape, then brings in CDC6. Kuhulika Bhalla, a postdoc in Stillman’s lab, explains:
“So if you can imagine a lava lamp, like you’ve got liquid, but you’ve got other colored liquid within it. And they still managed to stay separated.”
Throughout most of the cell division cycle, ORC1 and CDC6 amounts oscillate in the cell. Stillman explains that “both high and low amounts of ORC1 lead to severe consequences for cell viability. So, you have to have just the right amount” of each protein throughout the cell cycle. Stillman and his colleagues have shown that CDC6 recruits other regulatory proteins that control the activity and levels of ORC1 in both space and time. They published their findings in Molecular Cell.
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Materials provided by Cold Spring Harbor Laboratory. Original written by Jasmine Lee. Note: Content may be edited for style and length.

A study of young men with COVID-19 has revealed a genetic variant linked to disease severity.
The discovery, published recently in eLife, means that men with severe disease could be genetically screened to identify who has the variant and may benefit from interferon treatment.
For most people, COVID-19, the disease caused by the virus SARS-CoV-2, causes only mild or no symptoms. However, severe cases can rapidly progress towards respiratory distress syndrome.
“Although older age and the presence of long-term conditions such as cardiovascular disease or diabetes are known risk factors, they alone do not fully explain differences in severity,” explains first author Chiara Fallerini, Research Fellow in Medical Genetics at the Department of Medical Biotechnologies, University of Siena, Italy. “Some younger men without pre-existing medical conditions are more likely to be hospitalised, admitted to intensive care and to die of COVID-19, which suggests that some factors must cause a deficiency in their immune system.”
Recent research has suggested that genes controlling interferon are important in regulating the immune response to COVID-19. Interferon is produced by immune cells during viral infection. It works alongside molecules on the surface of immune cells called Toll-like receptors (TLR) which detect viruses and kickstart the immune response. “When a recent study identified rare mutations in a TLR gene, TLR7, in young men with severe COVID-19, we wanted to investigate whether this was an ultra-rare situation or just the tip of the iceberg,” says co-senior author Mario Mondelli, Professor of Infectious Diseases at the Division of Clinical Immunology and Infectious Diseases, Fondazione IRCCS Policlinico San Matteo and University of Pavia, Italy.
The team studied a subset of 156 male COVID-19 patients younger than 60 years old, selected from a large multicentre study in Italy, called GEN-COVID, which started its activity on March 16, 2020. GEN-COVID is a network of more than 40 Italian hospitals coordinated by co-senior author Alessandra Renieri, Full Professor of Medical Genetics at the University of Siena, and Director of Medical Genetics at Azienda Ospedaliero-Universitaria Senese, Siena, Italy.
The team first analysed all the genes on the X chromosome of men with both mild and severe cases of COVID-19, and identified the TLR7 gene as one of the most important genes linked to disease severity. They then searched the entire GEN-COVID database, and selected for younger men (less than 60 years old). This identified rare TLR7 missense mutations in five of 79 patients (6.3%) with life-threatening COVID-19 and no similar mutations in the 77 men who had few symptoms. They also found the same mutation in three men aged over 60: two who had severe COVID-19 and one who had few symptoms — although the mutation found in the man with few symptoms had little effect on TLR function.
To link these mutations to the immune cell response, they treated white blood cells from recovered patients with a drug that switches TLR7 genes on. They found that the TLR7 genes were dampened down in immune cells from patients with mutations, compared to the TLR7 activity seen in normal immune cells. They also found lower levels of interferon in the cells containing the mutation compared to normal white blood cells. This confirmed that the mutations identified directly affect the control of interferon as part of the innate immune response.
To confirm the impact of the mutations on COVID-19 response, the team studied two brothers, one with a mutation in an interferon gene and one without. The levels of interferon gene activity were much lower in the man with the missense mutation, compared with his brother. Moreover, the brother with the mutation had severe COVID-19, while his brother with normal interferon genes was asymptomatic.
“Our results show that young men with severe COVID-19 who have lost function in their interferon-regulating genes represent a small but important subset of more vulnerable COVID-19 patients,” says co-senior author Elisa Frullanti, Researcher of Medical Genetics at the University of Siena.
Co-senior author Alessandra Renieri adds: “These mutations could potentially account for disease severity in up to 2% of young men with COVID-19. We believe that screening for these mutations in men who are admitted with severe disease and promptly treating them with interferon could prevent more deaths.”
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Materials provided by eLife. Note: Content may be edited for style and length.

In the hours after we die, certain cells in the human brain are still active. Some cells even increase their activity and grow to gargantuan proportions, according to new research from the University of Illinois Chicago.
In a newly published study in the journal Scientific Reports, the UIC researchers analyzed gene expression in fresh brain tissue — which was collected during routine brain surgery — at multiple times after removal to simulate the post-mortem interval and death. They found that gene expression in some cells actually increased after death.
These ‘zombie genes’ — those that increased expression after the post-mortem interval — were specific to one type of cell: inflammatory cells called glial cells. The researchers observed that glial cells grow and sprout long arm-like appendages for many hours after death.
“That glial cells enlarge after death isn’t too surprising given that they are inflammatory and their job is to clean things up after brain injuries like oxygen deprivation or stroke,” said Dr. Jeffrey Loeb, the John S. Garvin Professor and head of neurology and rehabilitation at the UIC College of Medicine and corresponding author on the paper.
What’s significant, Loeb said, is the implications of this discovery — most research studies that use postmortem human brain tissues to find treatments and potential cures for disorders such as autism, schizophrenia and Alzheimer’s disease, do not account for the post-mortem gene expression or cell activity.
“Most studies assume that everything in the brain stops when the heart stops beating, but this is not so,” Loeb said. “Our findings will be needed to interpret research on human brain tissues. We just haven’t quantified these changes until now.”
Loeb and his team noticed that the global pattern of gene expression in fresh human brain tissue didn’t match any of the published reports of postmortem brain gene expression from people without neurological disorders or from people with a wide variety of neurological disorders, ranging from autism to Alzheimer’s.

A number of studies have shown that human coronaviruses, including SARS-CoV-2 which causes COVID-19, appear to attack neurons and the nervous system in vulnerable populations. This neuroinvasion through the nasal cavity leads to the risk of neurological disorders in affected individuals. Research conducted at the Institut national de la recherche scientifique (INRS) has identified ways to prevent the spread of infection within the central nervous system (CNS). The study, led by Professor Pierre Talbot and his research associate Marc Desforges, now at CHU-Sainte-Justine, was published in the Journal of Virology.
Antiviral immunity to human coronaviruses
The research team is the first to make the demonstration of a direct link between neurovirulence, protein S cleavage by cellular proteases and innate immunity. This antiviral immunity arises from the production of interferons, frontline proteins that help to detect early the presence of the virus.
“Using a common cold coronavirus, similar to SARS-CoV-2, we were able to show that cleavage of the S protein and interferon could prevent its spread to the brain and spinal cord in mice,” says Talbot, who has been studying coronaviruses for nearly 40 years.
Two therapeutic approaches
According to Marc Desforges, currently a clinical specialist in medical biology at the CHU-Sainte-Justine virology laboratory, the cleavage of the S protein by various cellular proteases is essential for these viruses to effectively infect cells and spread to various organs and systems in the body, including the central nervous system (CNS).
“Our results demonstrate that interferon produced by different cells, including olfactory receptors and cerebrospinal fluid (CSF) producing cells in the brain, could modulate this cleavage. Thus, it could and does significantly limit the viral spread in the CNS and the severity of the associated disease,” says the specialist who worked for 16 years as a research associate at the Armand-Frappier Health Biotechnology Centre of the IRNS.
Taken together, these results point to two potential antiviral targets: protein S cleavage and effective interferon-related innate immunity. “Understanding the mechanisms of infection and viral propagation in neuronal cells is essential to better design therapeutic approaches,” says Talbot. This is especially important for vulnerable populations such as the elderly and immunocompromised.” This discovery opens the door to new therapeutic strategies.
About the study
The article “Potential differences in cleavage of the S protein and type-1 interferon together control human coronavirus infection, propagation, and neuropathology within the central nervous system,” by Alain Le Coupanec, Marc Desforges, Benedikt Kaufer, Philippe Dubeau, Marceline Côté and Pierre J. Talbot, was published in the Journal of Virology. The study was supported by the Canadian Institutes of Health Research (CIHR).
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Materials provided by Institut national de la recherche scientifique – INRS. Original written by Audrey-Maude Vézina. Note: Content may be edited for style and length.

According to a recent Finnish study, accumulating more brisk and vigorous physical activity can curb adiposity-induced low-grade inflammation. The study also reported that diet quality had no independent association with low-grade inflammation. The findings, based on the ongoing Physical Activity and Nutrition in Children (PANIC) Study conducted at the University of Eastern Finland, were published in the European Journal of Sport Science.
The study was made in collaboration among researchers from the University of Jyväskylä, the University of Eastern Finland, the Norwegian School of Sport Sciences, and the University of Cambridge.
Low-grade inflammation is linked to many chronic diseases, but exercise can curb it
Long-lasting low-grade inflammation increases the risk for type 2 diabetes and cardiovascular diseases. Being overweight and obese contribute to low-grade inflammation, but little is still known about the role of lifestyle in curbing low-grade inflammation since childhood.
“Our study showed that children who were physically more active and less sedentary had a healthier inflammatory profile than children who were physically less active,” explains Dr. Eero Haapala from the Faculty of Sport and Health Sciences at the University of Jyväskylä. “However, our results suggest that the positive effects of high levels of vigorous physical activity and low levels of sedentary time on low-grade inflammation are partly explained by their positive effects on body composition.”
Low physical activity, unhealthy diet quality, and being overweight is the most unfavourable combination
Researchers found unhealthier inflammatory profile particularly in children with the lowest levels of physical activity, poorest diet quality and the highest body fat percentage.
“The key message of our results is that increasing physical activity and reducing sedentary time are key in preventing low-grade inflammation since childhood,” says Haapala. “They would be particularly important for overweight children.”
The study looked at the associations between physical activity, sedentary time, diet quality, body fat content, and low-grade inflammation in 390 children aged 6 to 8 years. Physical activity and sedentary time were measured by a combined heart rate and movement sensor and body composition with a DXA device. Low-grade inflammation was assessed using biomarkers measured from blood samples.
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Materials provided by University of Jyväskylä – Jyväskylän yliopisto. Note: Content may be edited for style and length.

It’s not just your legs and heart that get a workout when you walk briskly; exercise affects your brain as well. A new study by researchers at UT Southwestern shows that when older adults with mild memory loss followed an exercise program for a year, the blood flow to their brains increased. The results were published online today in the Journal of Alzheimer’s Disease.
“This is part of a growing body of evidence linking exercise with brain health,” says study leader Rong Zhang, Ph.D., professor of neurology at UTSW. “We’ve shown for the first time in a randomized trial in these older adults that exercise gets more blood flowing to your brain.”
As many as one-fifth of people age 65 and older have some level of mild cognitive impairment (MCI) — slight changes to the brain that affect memory, decision-making, or reasoning skills. In many cases, MCI progresses to dementia, including Alzheimer’s disease.
Scientists have previously shown that lower-than-usual levels of blood flow to the brain, and stiffer blood vessels leading to the brain, are associated with MCI and dementia. Studies have also suggested that regular aerobic exercise may help improve cognition and memory in healthy older adults. However, scientists have not established whether there is a direct link between exercise, stiffer blood vessels, and brain blood flow.
“There is still a lot we don’t know about the effects of exercise on cognitive decline later in life,” says C. Munro Cullum, Ph.D., professor of psychiatry at UTSW and co-senior author of the study. “MCI and dementia are likely to be influenced by a complex interplay of many factors, and we think that, at least for some people, exercise is one of those factors.”
In the study, Zhang, Cullum, and their colleagues followed 70 men and women aged 55 to 80 who had been diagnosed with MCI. Participants underwent cognitive exams, fitness tests, and brain magnetic resonance imaging (MRI) scans. Then they were randomly assigned to either follow a moderate aerobic exercise program or a stretching program for one year. The exercise program involved three to five exercise sessions a week, each with 30-40 minutes of moderate exercise such as a brisk walk.