Can We Actually Slow Down Ovarian Ageing?

The race to “rejuvenate” the ovary and what the science actually says.

For a long time, ovarian ageing has felt like one of those biological rules we simply cannot negotiate with.

Our ovarian reserve falls over time, and the eggs that remain age too.

But scientists are now asking a really interesting question: "Could we slow down some of that process?"

Researchers are studying everything from PRP injections and stem cells to mitochondria, NAD+ and drugs that target ageing cells.

Some of the science is genuinely exciting. Some of it is still very early.

And some of it is already being sold to women as “ovarian rejuvenation” long before we know whether it actually works.

So before we talk about rejuvenating an ovary, we need to understand what is actually ageing in the first place.

What actually happens when an ovary ages?

When we talk about ovarian ageing, most people think about one thing: running out of eggs. Oh well... that is certainly part of it.

The ovarian reserve (the pool of follicles capable of potentially producing mature eggs) is largely established before birth and declines throughout life. Most follicles never reach ovulation; the overwhelming majority are naturally lost along the way.

There is currently no established treatment that replenishes this reserve with a new supply of young, functional human eggs.

But ovarian ageing is not only about how many eggs remain. It is also about what happens to those eggs with time.

Human oocytes begin meiosis before birth and then spend years, sometimes decades, paused before completing that process around the time of ovulation.

That is biologically extraordinary but it also creates opportunities for things to go wrong.

As maternal age increases, chromosome-separation errors become more common.

One important mechanism appears to involve deterioration of cohesin (proteins that help hold chromosomes together correctly). Changes in the meiotic spindle, chromosome attachments, mitochondria, DNA integrity and other cellular systems are also being investigated.

The result is an increasing chance that an egg contains the wrong number of chromosomes, known as aneuploidy.

This is one major reason why fertility declines and miscarriage risk rises with increasing reproductive age.

The ovary around the egg is ageing too

An oocyte does not sit alone inside the ovary. It develops inside a follicle, surrounded by granulosa cells, blood vessels, immune cells, connective tissue, signalling molecules and an extracellular matrix that physically supports the tissue.

Scientists sometimes refer to this wider environment as the ovarian niche. And it changes with age.

Research also shows that the ageing ovarian stroma can become more fibrotic, inflammatory and mechanically stiff, while blood vessels, immune-cell behaviour, extracellular matrix composition and communication between ovarian cells can change too.

An ageing ovary is not simply a container with fewer eggs left inside.

As we age, the whole biological neighbourhood is changing. That is important. Because even if we cannot simply manufacture a fresh supply of young eggs, perhaps some parts of the environment surrounding the remaining follicles could eventually be modified.

And that is where the idea of “ovarian rejuvenation” begins.

But what does “rejuvenation” actually mean?

Imagine someone with diminished ovarian reserve receives an experimental treatment. Three months later, her AMH is higher. Her FSH is lower. An ultrasound shows more antral follicles.

Has her ovary become younger? Not necessarily.

AMH (anti-Müllerian hormone) and antral follicle count are useful tools for estimating ovarian reserve and, particularly in IVF, anticipating how strongly the ovaries may respond to stimulation but they do not measure egg quality or reliably tell us whether someone will become pregnant or have a live birth.

ESHRE's 2025 ovarian-stimulation guideline specifically recommends AMH or antral follicle count for predicting ovarian response, while stating that they should not be used to predict pregnancy or live birth.

This distinction is crucial because as treatment might temporarily change a hormone level. It might recruit follicles that were already there. It might even allow more eggs to be collected during IVF. But that does not automatically mean that those eggs are biologically younger, more likely to have the correct number of chromosomes or more capable of producing a healthy baby.

A major 2026 review of ovarian ageing makes the same point: improvements in AMH, follicle count, egg yield or menstrual function do not necessarily translate into improved oocyte competence, chromosomally normal embryos or live birth.

So whenever we hear the words “ovarian rejuvenation,” we should ask "Rejuvenated according to what?"

And with that in mind, let's look at what scientists are actually trying.

PRP: injecting the ovary with your own platelets

PRP stands for platelet-rich plasma and the basic idea behind it is surprisingly simple.

Blood is taken from the patient and processed in a centrifuge so that plasma containing a higher concentration of platelets can be collected. That plasma is then injected into the ovary.

Platelets are best known for their role in clotting, but they also contain and release growth factors and other signalling molecules involved in tissue repair and remodelling.

The theory is that introducing these signals into ovarian tissue might alter the ovarian environment and perhaps improve the response of remaining follicles.

It is biologically interesting. But clinically, the evidence is still weak.

Small studies have reported changes in AMH, FSH, follicle numbers and egg retrieval after PRP. The problem is that results are inconsistent, many studies are small or poorly controlled, and PRP itself is far from standardised.

Clinics can differ in how the blood is processed, platelet concentration, preparation method, dose and injection technique.

Most importantly, we still do not have convincing evidence that intraovarian PRP improves the chance of having a baby.

The UK's Human Fertilisation and Embryology Authority reviewed the evidence again in 2025 and published its updated assessment in February 2026.

For people with poor or diminished ovarian reserve, it currently gives intraovarian PRP a red rating for improving the chance of having a baby.

The HFEA states that there is no moderate or high-quality evidence showing that it improves treatment outcomes and highlights potential safety concerns including infection, bleeding, anaesthetic-related risks and trauma from injecting directly into the ovary.

This means that, for now, we simply do not have strong enough evidence to say that PRP has a proven role in improving reproductive outcomes.

What about stem cells?

Stem cells are another area researchers are exploring, especially mesenchymal stromal cells, which can be collected from tissues such as bone marrow or fat.

But the idea is not to inject stem cells and suddenly grow a whole new supply of eggs. We are nowhere near that.

What researchers are more interested in is the way these cells communicate with the tissue around them.

Mesenchymal stromal cells release signals that can affect inflammation, blood-vessel growth, fibrosis and the behaviour of nearby cells. So the hope is that, rather than creating new eggs, they might help improve the environment around follicles that are already there.

There have been some interesting early findings in humans, but the evidence is still very limited and stem-cell approaches remain experimental.

A recent systematic review looked at 27 human studies involving 694 patients with premature ovarian insufficiency or poor ovarian response. The problem? Nearly 78% of those studies had no control group.

That makes it very difficult to know whether the changes seen were actually caused by the stem-cell treatment, or whether something else was going on.

A 2026 conference study involving 48 women with very poor ovarian response also reported temporary hormonal changes and signs of follicular recruitment after treatment with stem cells derived from fat tissue.

Again, though, there are important limitations. The study was small, retrospective and not a randomised controlled trial. Even the researchers themselves described the response as time-limited.

So... yes, the results are interesting but they do not form proof that stem cells can reverse ovarian ageing.

Then we get to the mitochondria

Mitochondria are tiny structures inside our cells that help produce the energy the cell needs to function.

And eggs need a lot of it.

An oocyte has to mature, organise and separate its chromosomes correctly, be fertilised, and then help support the embryo during its earliest stages of development.

As eggs age, their mitochondria change too. They can become less efficient, energy production can be affected, and changes can also appear in mitochondrial DNA.

So researchers started to explore a very simple question: if ageing eggs have problems with their mitochondria, could giving them healthier ones help?

What if we gave an ageing egg healthier mitochondria?

That question led researchers to test something called autologous mitochondrial transfer essentially adding extra mitochondria from the same patient into an egg during ICSI.

One of the first approaches, called AUGMENT, attracted a lot of attention because the idea made biological sense.

But when it was tested in a randomised pilot study, the results were disappointing. It did not improve the patients' reproductive outcomes, and the treated eggs actually produced fewer blastocysts in that study.

Researchers kept exploring the idea...

In 2026, another trial looked at mitochondria taken from the patients' own bone-marrow mesenchymal stromal cells. The study included 151 patients and 1,178 mature eggs, with sibling eggs randomly assigned to either mitochondrial transfer or standard ICSI.

The extra mitochondria did seem to change the timing of some of the embryo's earliest cell divisions.

But when researchers looked at the main outcome they were interested in (the number of good-quality embryos on day three) there was no improvement.

The study also reported pregnancy and live-birth outcomes, but those comparisons need to be interpreted more carefully because they were not fully randomised at the patient level.

So once again, we see the same pattern... the biology changed, but the clinical benefit was not clearly there...

And that distinction really matters.

Changing what an embryo does in the lab is not the same as proving that it is more likely to develop into a healthy pregnancy or result in a live birth.

It is also worth separating this from another type of mitochondrial treatment that sometimes gets grouped into the same conversation.

Mitochondrial transfer being explored as a way to improve fertility is not the same as mitochondrial donation or mitochondrial replacement therapy, which has a completely different purpose: reducing the risk of passing on certain serious mitochondrial diseases from mother to child.

The techniques may sound similar because both involve mitochondria, but they are being used to answer very different medical problems.

And then there is NAD+

If you have spent any time reading about longevity, you have probably come across NAD+.

NAD+, short for nicotinamide adenine dinucleotide, is a molecule our cells rely on for things like energy production, mitochondrial function, DNA repair and responding to cellular stress.

And, like many other things in the body, NAD+ metabolism changes as we age.

That has made it an obvious target for researchers studying ovarian ageing.

Scientists have been particularly interested in compounds that can boost NAD+ levels, including precursors such as NMN and NR.

In ageing mice, increasing NAD+ availability has been linked to improvements in mitochondrial function, oocyte quality and, in some studies, reproductive outcomes.

And you can probably already see where the headline goes:

Could boosting NAD+ help keep eggs younger for longer?

The problem is that we are missing one very important part of the story: women.

A major review published in Biology of Reproduction in 2026 concluded that our understanding of NAD+ metabolism in the human ovary is still developing, and that well-designed human clinical studies directly testing NAD+ targeted fertility treatments are still lacking.

So at the moment, we simply do not know whether taking NMN, NR or another NAD+ boosting supplement can actually slow ovarian ageing, improve egg quality in women or increase live-birth rates.

We also do not yet fully understand the long-term reproductive effects or safety of chronically manipulating these pathways.

So for now, the fairest conclusion is: Interesting mechanism? Yes. Promising animal data? Yes. Proven anti-ageing treatment for human ovaries? No.

Could we remove ageing cells instead?

Then there are senolytics.

As we age, some cells enter a state called cellular senescence. They stop dividing, but they do not simply disappear. They stay in the tissue and can release inflammatory and signalling molecules that affect the cells around them.

These senescent cells build up in many ageing tissues, and researchers think the ovary may be no exception.

That has led to the idea that is worth exploring what would the outcome be if we could selectively remove some of these ageing cells.

This is where senolytics come in. They are drugs being studied for their ability to target certain senescent cells.

In animal research, the idea is genuinely exciting.

But when it comes to ovarian ageing in women, we are still very early.

There is currently no established senolytic treatment proven to preserve egg quality, delay menopause or extend fertility.

And there is another reason why this is not as simple as just getting rid of every ageing cell.

Senescence is not always harmful. These cells can also play useful roles in things like tissue repair, development and protecting against cancer.

So the real challenge is to identify which senescent cells are actually causing harm. When should they be removed? And would removing them really improve fertility?

Right now, we simply do not know.

Maybe the real target isn't the egg

For a long time, most of the attention was on the egg itself.

But an egg does not age in isolation.

The blood vessels around it change. The cells supporting it change. The tissue becomes more fibrotic. Inflammation, metabolism and the way cells communicate with each other can all shift with age.

So researchers are starting to look at the bigger picture.

What if the goal is not to somehow make an older egg young again?

What if, instead, we could keep the environment around that egg healthier for longer?

That might mean improving the way follicles are supported, reducing harmful changes in the surrounding tissue or helping the ovary function better as it ages.

So is there anything we can actually do today?

For now, the most effective things we can do are mostly about preserving fertility or working around ovarian ageing, rather than reversing it.

Egg freezing is probably the clearest example.

If eggs are collected and frozen at a younger age, they keep the biological age they had when they were retrieved. Your ovaries will keep ageing, but the eggs in storage do not age along with you.

That can be especially important for someone about to have chemotherapy or another treatment that could affect fertility, where options may include freezing eggs, embryos or, in some cases, ovarian tissue.

So, can we slow ovarian ageing?

Not in the way “ovarian rejuvenation” is often sold.

Right now, we cannot make an ovary biologically young again, replace a depleted ovarian reserve with new eggs, or take a supplement proven to reverse egg ageing.

But the answer is not completely no either.

Researchers are starting to understand the individual processes behind ovarian ageing, from mitochondrial dysfunction and inflammation to fibrosis, metabolism and cellular senescence.

Some of those pathways may eventually become targets for treatment.

We just do not yet know whether changing them will actually lead to better fertility outcomes or more healthy babies.

So for now, this is the distinction worth remembering:

A higher AMH does not necessarily mean a younger ovary. More follicles do not necessarily mean younger eggs. And changing a marker is not the same as changing the outcome.