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.

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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.”

We used to think that once ovaries had passed through the menopausal transition, the scarred, shrunken organs sat inert in the body. But the discovery that the ovaries of aged mice become infiltrated with immune cells suggests the organ may be linked to widespread inflammation after menopause.

“We assumed the organ had done its job [post-reproduction],” says at Northwestern University in Illinois. “What we found was super surprising.”

In March, Duncan and her colleagues published a , which hasn’t yet been peer reviewed, looking at the protein composition of ovaries in post-menopausal women aged 50 to 75. They expected all the ovaries to be fairly similar, but instead Duncan found their “molecular signatures changed quite dramatically over the decades, which told us: this organ is not stagnant, it’s changing over time”.

To better understand what happens, Duncan and her team have now studied the ovaries of mice in more detail. They analysed the tissue and gene expression within the ovaries of young (aged 2 months), reproductively old (18 months) and post-reproductive (24 months) mice.

Mice don’t have a menstrual cycle like us – their uterus lining is reabsorbed, not shed as a period. They also don’t go through the menopause like we do, but their egg reserves deplete with age and their cycles become irregular. “What we are referring to when we talk about menopause is the age-related decline in fertility and [hormonal] function, and mice absolutely go through that same thing,” says Duncan.

Some of the results were expected: the older ovaries lost their egg-producing follicles, for example, and showed more scarring. What’s more, genes involved in reproduction and the creation of hormones like estradiol, a form of oestrogen, were downregulated. But the team also found that genes linked to inflammation and immune activity became increasingly active, and the number of immune cells in the ovaries, including T cells and macrophages, increased with age.

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Further research is required to uncover what this may mean for immune – and overall – health, but Duncan suspects this represents an identity change for the ovaries, rather than them becoming “an immune superpower”. “[The ovaries are] losing sort of the reproductive signature and taking on an immune signature, but I don’t think that’s necessarily a good thing.”

Ageing tissues undergo “inflammaging”, a state of chronic, low-grade inflammation. Immune cells are heavily involved in this, which makes Duncan suspect that post-reproduction, ovaries contribute by releasing inflammatory signalling molecules. “It is possible [this post-reproductive change] means nothing, but it’s also possible it’s sending out these signals and communicating with other parts of the body,” she says.

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Duncan stresses the study was only in mice, but at the University of California, San Francisco, suspects similar immune changes occur in humans, given . “Both organisms cease cycling when their supply of oocytes [immature egg cells] dips below a critical threshold, and other changes including fibrosis and increased innervation [nerve distribution] are shared,” she says.

It is unclear why ageing mice may have evolved this change in signature, says Duncan, but if the same change applies to humans, it could have been an advantage to acquire an immune cell reservoir when fewer people lived to old age. But this may lead to inflammation and even autoimmune conditions in modern life.

The findings raise questions about the importance of the ovaries post-menopause. If healthy, they are generally left in place because they , which help maintain bone mineral density and libido. But Laird says the study adds to growing evidence that that causes issues like rheumatoid arthritis post-menopause. “The findings are a call to carry out detailed and functional studies on the cellular and molecular components of the post-reproductive ovary,” she says.

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