The experimental drug combo dasatinib and quercetin (known for short as D+Q) is one of the most promising anti-aging therapies being developed right now.

It is not yet approved for human use, but some scientists think it has the potential to fight disease by improving how our systems clear out worn-down cells.

According to a new study, however, there might be a big problem with D+Q.

A team from the University of Connecticut tested D+Q on the brains of mice, and discovered it caused serious damage to the myelin insulation wrapped around nerve fibers.

The effects of D+Q on the central nervous system haven't been extensively tested before, which was part of the motivation behind this new study.

The findings raise questions about widespread clinical use.

Various clinical trials for D+Q are already underway, for conditions such as kidney disease and pulmonary fibrosis.

Because of the hype, the experimental drug combo is even taken by some people without a prescription, as part of an unofficial 'anti-aging' regime.

That is something medical professionals warn against, as the drug combos have not yet been properly tested for safety or efficacy in humans.

"When you administer this cocktail to an animal, young or old, the myelin is damaged, which makes it disappear – even worse in the young animals than in the aged ones," says immunologist Stephen Crocker.

There are similarities between the brain damage observed here and the effects of both multiple sclerosis and something called 'chemo brain', where chemotherapy treatments lead to problems with cognitive function.

Dasatinib, on its own, is an essential medicine used to treat cancer, sometimes alongside chemotherapy, which might help explain what's causing the myelin loss.

When myelin is degraded, nerves can't communicate as efficiently, and much of the damage observed in the brains of mice was focused around a major information highway called the corpus callosum.

Further lab tests analyzed the reaction between D+Q and oligodendrocyte brain cells, which help grow and maintain myelin.

Tests showed that the combo drug treatment apparently caused oligodendrocytes to shrink back to a smaller and younger mode of operation.

There were changes in the metabolism of the oligodendrocytes, too, preventing enough myelin from being produced, and leaving nerves exposed.

While these results are only from a small number of animals rather than humans, there's definitely enough here to be concerning.

Further analysis is now definitely warranted – in monitoring brain cells during clinical trials of D+Q, for example.

"We suspect the drugs are choking off energy the cells need, and the cells respond by reducing complexity, reverting to a younger state, but less functional," says Crocker.

What makes D+Q exciting for scientists is that they act as senolytics, which are drugs that deliberately clear out damaged or old cells.

These dysfunctional cells are known as senescent cells, and they build up as we get older. Their presence in the body triggers inflammation, which may be related to a host of different diseases, including multiple sclerosis and Alzheimer's disease.

If senolytics like D+Q can reduce the senescent cell burden, then the potential impact on anti-aging diseases is immense.

The aging process is related to so many aspects of health, which is why so much research is dedicated to trying to slow it down.

But there is still much work to be done before that reality is realized.

Based on these new findings, caution moving forward is warranted.

There is some positive news to take out of this research among mice, though.

The stressed-but-still-alive oligodendrocytes are similar to cells seen in patients with multiple sclerosis.

This means D+Q could be used in lab tests to figure out what treatments might work best for reversing some of the damage done by the autoimmune condition.

Related: These Popular Supplements Are Sold With Anti-Aging Claims. Here's What Science Says.

"If we can mimic this, we have an amazing opportunity to see if the cells can recover and repair the brain," says Crocker.

The research has been published in PNAS.

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Researchers have made a significant step forward in understanding how gut bacteria, and specifically a newly discovered virus, can contribute to one of the most common forms of cancer in the developed world.

Scientists from institutions in Denmark and Australia wanted to take a closer look at a previously identified association between colorectal cancer and a bacterium called Bacteroides fragilis.

B. fragilis often shows up in healthy people too.

"It has been a paradox that we repeatedly find the same bacterium in connection with colorectal cancer, while at the same time it is a completely normal part of the gut in healthy people," says microbiologist Flemming Damgaard, from Odense University Hospital in Denmark.

The team wanted to see if there was a crucial difference in the bacterium in individuals who develop cancer – and that's exactly what they found.

"We have discovered a virus that has not previously been described and which appears to be closely linked to the bacteria we find in patients with colorectal cancer," says Damgaard.

Using genetic sequencing, the researchers analyzed the gut bacteria of cancer patients in a large Danish population study.

They found that in these patients, B. fragilis often carried a bacteriophage.

Bacteriophages are viruses that live inside bacteria, hijacking these cells to duplicate and spread.

While the initial signal was discovered in a relatively small group of people, the findings were later verified in a larger cohort of 877 people with and without colorectal cancer – and point to a link that suggests viruses lurking in B. fragilis may tip the scales toward cancer.

People with colorectal cancer were twice as likely to have detectable levels of the bacteriophage in their gut bacteria, the data showed. What's more, it's not a virus that fits the description of anything recorded to date.

However, the researchers can't prove a direct cause-and-effect relationship yet. This is a notable association that will be useful for studying colorectal cancer and potential treatment targets, but there may be much more going on.

"It is not just the bacterium itself that seems interesting," says Damgaard.

"It is the bacterium in interaction with the virus it carries."

"We do not yet know whether the virus is a contributing cause, or whether it is simply a sign that something else in the gut has changed."

Around 80 percent of colorectal cancer risk has been assigned to environmental factors, including gut bacteria composition. That means a better understanding of these factors and how they influence one another could affect millions of cancer cases.

Studying the mix of bacteria in the gut is no easy task.

These incredibly complex microbiomes are both indicators of what else is going on in the body and influencers that can impact everything from sleep quality to weight loss.

Now there's an extra layer that future studies can examine: not just bacteria, but the viruses living inside them. One question the researchers are keen to look at next is exactly how B. fragilis might be affected by its bacteriophage lodgers.

This research is still very much in the early, experimental stage, but anything that helps experts understand how cancer starts could potentially also help develop targeted treatments – though that may take years.

"The number and diversity of bacteria in the gut is enormous," says Damgaard.

"Previously, it has been like looking for a needle in a haystack. Instead, we have investigated whether something inside the bacteria – namely viruses – might help explain the difference."

The team suggests that their findings might also be used for colorectal cancer screening. With further research, stool sample scans could be developed to look for this B. fragilis virus, for example.

Related: Colorectal Cancer Is Rising in Young People. Here's How to Lower Your Risk.

"In the short term, we can investigate whether the virus can be used to identify individuals at increased risk," says Damgaard.

The research has been published in Communications Medicine.

An earlier version of this article was published in February 2026.

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