The best treatment for multiple sclerosis (MS) might be antivirals that target the Epstein-Barr virus. Pharmaceutical companies are now being called on to develop such drugs after researchers studied the immune responses of people with and without the condition.

“There aren’t good Epstein-Barr virus drugs currently available, but they can be developed,” says at Harvard Medical School. “That might be the most useful specific therapy for MS in the future.”

MS is caused by an immune attack on myelin, a fatty sleeve that wraps around nerves. The loss of myelin reduces their ability to transmit signals and can cause a wide range of symptoms, including muscle weakness. Drugs that suppress the immune system can slow the progression of the condition.

There is strong evidence that the Epstein-Barr virus (EBV), which causes mononucleosis, or glandular fever, is also the cause of MS. “I think most MS researchers now would agree that EBV plays a major role in the development of the disease,” says team member at the Harvard T.H. Chan School of Public Health.

But exactly how remains a mystery. Almost everyone is infected with EBV during their childhood or teen years. It mainly infects immune cells known as B-cells, where it can remain dormant for the rest of a person’s life. But in some cells, the virus can reactivate.

The big question is why only around 1 in 1000 people develop MS when nearly everyone gets EBV. This suggests there is something different about the immune response to EBV in people who go on to develop MS, says team member at Massachusetts General Hospital. “Our question for this study was: in people with MS, what parts of EBV does the immune system respond to? And do those responses look different from people who don’t have MS?”

The team focused on immune cells known as CD4 T-cells, which circulate in the body. Although these aren’t the cells that directly attack myelin, there are multiple lines of evidence suggesting they play a role in MS, says Drosu.

The team found that, in 30 people with MS, most of the CD4 T-cells targeting EBV were specifically targeting viral proteins produced when the virus is actively replicating, rather than the proteins associated with its dormant stage. What’s more, people with MS produced twice as many of these cells, on average, as 30 people without the condition.

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The researchers then looked at CD4 T-cells in 60 people with MS before and after they began drug treatments that reduce their number of B-cells. They found these treatments reduced the T-cell response to EBV almost to the levels seen in people without MS.

In addition, the team found low levels of EBV in the saliva of these people before they were treated to reduce their number of B-cells, which shows that the virus was replicating in their bodies. After treatment, viral levels dropped below detectable levels in most people.

The thinking has been that B-cells help drive the harmful immune response in people with MS, says Levy, and this is why drugs that reduce B-cell levels are effective. But the results suggest these drugs also work by eliminating B-cells infected with EBV, he says, thereby reducing the immune response caused by active viral replication. “We’re thinking that depleting B-cells is also depleting the reservoir of the Epstein-Barr virus.”

If so, targeting EBV directly with antivirals might be just as effective as B-cell-depleting drugs, but without the undesirable side effects of treatments that weaken the immune system, such as an increased risk of infections. “I think a lot of patients would prefer a specific drug,” says Bjornevik. “If we can show that an antiviral had a similar effect as the most effective MS drugs, I think there will be a big market for that drug.”

Another approach already being trialled for treating MS is using modified immune cells called CAR T-cells. While existing drugs merely reduce B-cell levels, CAR T-cells can temporarily eliminate them altogether. Dozens of people with MS have gone into remission after CAR-T treatment, says Levy.

Strongest evidence yet that the Epstein-Barr virus causes lupus

Lupus has been linked to the Epstein-Barr virus – which causes glandular fever, or mono – before, but we now have evidence of how it can bring about the autoimmune condition

But EBV might linger in some other cell types and reinfect B-cells as they slowly recover in the years after the CAR T-cell treatment, he says. “Then we would need the antivirals… so we just have to wait and see.” CAR T-cells can also have serious side effects, says Bjornevik, so antivirals could be safer as well.

There are also vaccines against EBV under development. “If people don’t get infected with EBV, their risk of MS would be virtually zero,” says Drosu. “So I think vaccines are [a] very promising strategy to eradicate MS.”

But 1000 people would have to be vaccinated to prevent just one case of MS, Levy points out. However, EBV causes many other problems, including a number of cancers, and has also been linked to other autoimmune conditions, such as lupus and rheumatoid arthritis.  

A cognitive “speed training” game that cuts dementia risk by 25 per cent alters levels of beta-amyloid, a protein that clogs up the brain in Alzheimer’s disease, in men, but not in women.

It is the first time brain training has been shown to influence the levels of a neurodegenerative marker, strengthening the evidence suggesting that mental exercises can boost brain health.

“One of the main markers that’s indicative of future dementia risk got better for men who completed cognitive speed training,” says  at Clemson University in South Carolina, who presented the research at the Alzheimer’s Association International Conference in London on 12 July.

The computer-based speed training involves recalling where objects have flashed up, with the task becoming harder as performance improves. A prior 20-year study by some of Chai’s colleagues showed that people aged 65 and older, who did the training were 25 per cent less likely to be diagnosed with Alzheimer’s disease or a related form of dementia compared with a control group.

In the latest study, Chai and her team recruited a separate group of 53 people from the US aged 65 and older, 13 of whom were male. About a third of the participants were asked to complete between 2 and 4 hours of speed training each week for 4.5 months.

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The remaining participants were either told to spend the same amount of time playing games such as Solitaire, word search and a game similar to Connect 4, or to complete another kind of brain training in which they had to strategically track objects and switch between tasks.

To explore how speed training may reduce dementia risk, the team collected blood samples from all of the participants at the start and end of the training period.

This revealed that, among men, speed training increased the ratio of two forms of beta-amyloid found in the blood, which suggests the training boosted the brain’s ability to clear beta-amyloid 42. This protein forms clumps called plaques in the brain during Alzheimer’s disease, disrupting brain function. The other two kinds of training had no effect.

“It’s a really cool finding,” says  at McGill University in Montreal. “It is definitely strengthening what they’ve [previously] shown with the reduction in dementia.”

Some Alzheimer’s treatments, such as lecanemab, have been designed to help clear amyloid from the brain, but they only marginally slow cognitive decline during Alzheimer’s disease. The limited benefit seen in trials is probably down to these treatments being taken at a relatively late stage of the condition, when substantial brain damage has already occurred, says at University College London.

Engaging in cognitive training to reduce beta-amyloid build-up before dementia develops may have a bigger effect on dementia because it would be done before much brain damage has occurred, says Castegnaro.

However, cognitive training had no effect on amyloid levels in female participants in the study. This suggests that speed training reduces dementia risk in different ways in women and men, says Chai.

The team hopes to explore how speed training may benefit women in future studies, says Chai. But first, the findings need to be verified in geographically and ethnically diverse groups, says Novozhilova.

Human eggs that contain too many or too few chromosomes can lead to miscarriage, IVF failure and conditions such as Down’s syndrome. Now, researchers have found that giving the eggs a single injection can substantially reduce the risk of chromosome error. The approach could eventually boost the chances of success for older women undergoing IVF.

“It really seems like a big deal,” says at Nilo Frantz Reproductive Medicine in Porto Alegre, Brazil, who wasn’t involved in the new research. “To my knowledge, this is the first [therapy] to show such clinical potential for correcting this major cause of IVF failure.”

During a process called meiosis, egg and sperm cells eject exactly half of their genetic material. This means that when egg and sperm combine during fertilisation, they form an embryo with a complete genome. Sometimes, however, a sperm or egg cell has slightly more or slightly less than the half genome it should contain. This is a condition known as aneuploidy.

Aneuploidy affects about in the early 30s and becomes more common with age. “Already in the late 30s, more than 65 per cent of all eggs are aneuploid,” at Ovo Labs, a biotechnology company in Germany, told the audience at the conference in London on 6 July.

Clinicians sometimes screen IVF embryos for aneuploidy when treating couples at greater risk of miscarriage or IVF failure. , conditions caused by the genetic error – which include Down’s syndrome – are only detected via blood tests and ultrasound scans taken during the first trimester of pregnancy. Until now, there have been no ways to reduce the risk of aneuploidy occurring in the first place, says Zielinska.

Now, Zielinska and her colleagues have found that the level of a protein called shugoshin-1 is substantially lower in older mouse and human eggs than in younger ones. Shugoshin-1 helps with a stage of meiosis in which two copies of each chromosome line up along the middle of an immature egg cell. The protein maintains the molecular glue that holds each pair together.

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When sperm penetrate an egg, the two copies of the egg’s chromosomes separate and move to opposite sides of the cell. One end ultimately forms the final egg cell, and the other end is discarded.

But in older eggs, the glue holding the chromosome pairs together degrades, which can cause the two copies of each chromosome to separate before fertilisation. When this happens, the chromosomes spread unevenly throughout the cell – which means the resulting egg may be aneuploid.

To explore whether replenishing shugoshin-1 could prevent aneuploidy by helping to hold chromosome pairs together, the team collected 111 spare, immature eggs from more than 30 women aged between 22 and 43 who were banking eggs or undergoing IVF.

The team injected the genetic code for shugoshin-1, in the form of mRNA, into one or more of each donor’s eggs, and left other eggs from the same donor untreated.

A few hours later, chromosomes had prematurely separated in 53 per cent of the untreated eggs, whereas this figure was nearly half – 29 per cent – in the treated ones. In eggs from nine donors who were aged over 35, aneuploidy rates were 65 per cent, on average, in untreated eggs. But in treated eggs, the average figure was just 44 per cent. This reduction wasn’t statistically significant, although this is probably because of the study’s small sample size, according to the researchers.

Common IVF test misses some genetic abnormalities in embryos

Human embryos formed with in vitro fertilisation can develop genetic abnormalities in the time between genetic testing and implantation – though this may not affect their viability

Further experiments showed the approach could prevent aneuploidy in mouse eggs, which were then successfully fertilised to produce healthy offspring.

No side effects were seen in the mouse or human studies. “We’ve achieved live births in mice, so, from that perspective, we’re confident that this approach is not interfering in the mouse model with any steps of embryo development, and it doesn’t interfere with pup health and pregnancy health,” Zielinska told the conference audience.

The researchers are now working towards testing the effects of shugoshin-1 in people. This would involve tweaking standard IVF to use immature eggs rather than mature ones, but this change would be fairly easy to implement, says Zielinska.

She hopes the therapy, which the team calls EmbryoProtect, will provide an affordable way to improve IVF for older women. “We anticipate that the treatment will cost a fraction of the cost of a full IVF cycle,” says Zielinska. “By meaningfully improving IVF success rates, especially for women over 35 where baseline success is low, we hope that fewer attempts will be needed to conceive.”