Microbiome links to Parkinson's, and a massive laser boost

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The Naked Scientists
Microbiome links to Parkinson's, and a massive laser boost
Microbiome links to Parkinson's, and a massive laser boost
Plus fast turnaround bacterial infection diagnostics, and the ill-health burden of nursery on parents and toddlers...
23 April 2026
Presented by
Chris Smith
.
Production by
Rhys James
,
Rachael Ralph
.
LASER-POWER-BOOST.jpg
Credit:
Image courtesy of Robin Timmis
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This week scientists confirm the link between changes to the microbiome and later development of Parkinson's Disease, a super speedy microfluidic way to diagnose infection and probe antibiotic susceptibility, how many infections does daycare cause in your toddler, and the breakthrough capable of boosting laser power by orders of magnitude...
In this episode
00:58 - Microbiome changes predict Parkinson's Disease
Might the microbes in the gut be kick-starting the inflammatory process that leads to Parkinson's?
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Microbiome changes predict Parkinson's Disease
Tony Schapira, UCL
Scientists in London have found that changes to microbes in the gut can identify people who are at greater risk of developing Parkinson’s disease. The study - which has been published in Nature Medicine - profiled the microbiomes of people with Parkinson’s, people at high genetic risk of developing the condition, and members of the general public with some early signs that they were developing the disease. It suggests that changes to gut microbes might cause or at least contribute to the disease becoming clinically manifest, possibly by altering our biochemistry or pushing up levels of inflammation around the body. Previously, it wasn’t clear whether gut changes were happening secondarily as a consequence of having Parkinson’s Disease. The new findings could help doctors to spot patients at higher risk of the neurodegenerative disorder, and even offer a new way to intervene. Speaking with Chris Smith, Tony Schapira is professor of neurology at UCL…
Tony - In our study, we found that there's a very distinctive signature, if you like, of the microbiome bacterial population in Parkinson's disease. We see this irrespective of whether the person has just been diagnosed or whether they're on drugs or not. So it's very specific for Parkinson's disease. And what we also found is that a small proportion of the general population have the same signature. And when we look at them very carefully, we can see some of the very earliest signs of Parkinson's disease. And then finally, we looked at a group of people who carry a gene for Parkinson's disease, and we found the same in them. So the outcome really is that we found an evolution, if you will, of the microbiome bacterial signature from normal general population through to those genetically at risk, and finally into those that have the disease.
Chris - Is the change to the microbiome the canary in the coal mine, or is the microbiome actually doing something to the disease process?
Tony - Yeah, so there's good evidence already that a change in the microbiome, and in particular a lack of diversity, can result in the overgrowth of certain bacteria that produce harmful chemicals in the gut, because all the bacteria in the gut are chemically active and living. And a proportion of those may produce chemicals that promote inflammation in the gut, that then can transmit that inflammation to the brain and produce some of the changes that may be at the earliest stages of Parkinson's disease. So there is a direct link between what may happen in the gut and what may happen in the brain.
Chris - In Parkinson's though, at least initially, a very specific population of nerve cells deteriorate, decline, and then are lost. So why would those nerve cells be selectively vulnerable to an inflammatory effect from the gut that, in theory, affects the whole body?
Tony - A good question to which we don't yet have an answer. The connection from the gut goes through the Vagus nerve to the brain. So there is a proximity, if you like, of the link between the gut and the brain, whereby certain chemicals or inflammation may be transmitted directly from the gut. But why that specific population of cells starts to die first, we don't yet know. We suspect it might be because they're particularly vulnerable because they're so active. So anything that disturbs their environment causes them a problem.
Chris - How did you actually do this study though? Because people have pointed the finger at the microbiome in association with Parkinson's in the past, but we've never known whether something causes Parkinson's and then causes a gut problem, or whether it's the other way around. You appear to have a bit more evidence that things do perhaps begin in the gut to start with. But how did you actually do the study?
Tony - So we were careful in the populations that we chose for study. So we took people from the UK and from Italy with Parkinson's disease, general population people, and those with a genetic predisposition. We also worked with people in France to develop a new way of looking at the microbiome in terms of how it can develop and shift over time. And we were able to confirm our findings in people in the United States, South Korea and Turkey.
Chris - And presumably these people who are living in different geographies, they're going to be slightly genetically different, but they're also going to be eating different things and living in a different environment. So if it all converges on a similar microbiome change, despite those other differences, that does add extra weight behind your argument, I presume?
Tony - I think so. Although these other populations were not studied in as much detail as ours, and we don't have the way in which they ate their food - their different dietary components - we assume the diet was generally different. However, in our populations, we found that the signature and the severity of the disease was very clearly linked to the quality of the diet that the people in our study ate. So a good diet, rich in fibre etc, reduced their risk of Parkinson's disease; whilst a poor diet increased the risk. And that was a result that ran across all of our populations under study.
Chris - If the microbiome does lie upstream of Parkinson's in the way that this appears to suggest it does, how far in advance do you get changes in the microbiome? And could that therefore be used as a predictor for who might be at risk? That's my first question. And the thing I'm going to follow on with is, well, if you know that, can we change it and change the outcome?
Tony - The results from the study suggest that if we can see the signature in a small proportion of people in the general population, we must think that they are at risk. And that is supported by the same finding in those genetically at risk and quite close to the development of the disease. So the answer is probably that we can use this microbiome several years in advance and before the onset of the disease to identify those who might be at risk. And in answer to the second question, this is the key, of course: can we change that microbiome signature to reduce an individual's risk of Parkinson's disease? The simple answer is probably yes, we can change the microbiome signature through a change in the diet. Whether that then reduces that person's risk of Parkinson's disease is something that will need to be tested in further studies. But I think at least based on the data that we have, should have a good chance of doing so...
08:44 - Speedy bacterial infection diagnostics
A new microfluidic technique watches bugs grow to make an infection diagnosis in a fraction of the time...
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Speedy bacterial infection diagnostics
Oliver Hancox, Astratus Limited
Urinary tract infections, or UTIs, are extremely common in the UK, accounting for 3% of all GP consultations and over 200,000 emergency hospital admissions annually. Part of the challenge is that it also takes a relatively long time for the bacterial cause of a urine infection to be identified, and an appropriate, narrow spectrum antibiotic specific for that bug to be selected. As a result, doctors tend to play it safe and over-treat UTIs, often with broader spectrum, more expensive agents, which drives up costs and rates of antimicrobial resistance. Now a new technology is hoping to change this. Astratus, a spin-out company from the University of Reading, has a microfluidic system that grows bacteria from patient samples in tiny volumes, watching how the microbes respond to different antibiotics. It can produce a diagnosis - and an antibiotic sensitivity - in under 6 hours. Better still, it should be ready to roll within the next couple of years. Speaking with Chris Smith, Oliver Hancox is their CEO…
Oliver - If we start with antimicrobial resistance as a top level problem, this is when we give an antibiotic to treat a bacterial infection and the drugs are no longer effective. In this case, we're dealing with one of the most prevalent bacterial illnesses going, so urinary tract infections. It affects more than 30% of our population and currently it takes up to three days to return a clinical result. So how do we make that faster? And what we've got here is a platform and a mechanism to take that test that takes three plus days and give a same day actionable results. And we can link that right drug with the right bug, importantly, at the right time.
Chris - Tell us how it works. What have you done to do that?
Oliver - We call ourselves pragmatic microfluidics. So we're looking at a very small amount of liquid, so one microlitre in this case, so a thousandth of a mil. And we're looking at bacterial growth within that physical growth. We're also able to look at it in response to some metabolic indicators that then tell us whether there's been bacterial growth in response to those drugs that we're exposing them to.
Chris - So, in practical terms then, you would, say, have a urine specimen; you'd need a tiny volume and you're able to watch the microbes that are causing what we think is potentially an infection there in real time growing and you can expose them to a host of different drugs and see which ones do and don't work.
Oliver - Yeah, exactly. So we take a panel of these antibiotic drugs, and as you say, monitor that bacterial growth in real time in response to those drugs, and then out of that map their growth or no growth and then give an accurate result out of that.
Chris - How do you actually monitor the growth though? How do you see these microbes are growing, these ones are not?
Oliver - The bacterial growth will then cause, in this case, an optical change. And we can then monitor that optical change and give a curve to then say there's either been bacterial growth here, we see an optical change or a colour change, or in this case, we don't see it if there's no colour change. And then we also look at physical bacterial growth itself.
Chris - Is that because the microbes just change the characteristics of the light you're looking at them with, or are they actually eating something that you've put there that produces a colour that enables you to see them?
Oliver - A little bit of both actually. We do some metabolic indicators, in which case the bacteria, through physical bacterial growth and activity, cause a colour change in some metabolic indicators, and that gives us a colour change that we're able to see. And when we also look at their physical mass, so the more bacteria grow, the more we're able to see them, because we're looking for them in a very small area, we're able to monitor that growth and categorise that as growth or no growth and the amount of growth that goes along with that.
Chris - Does it work for all different kinds of bacteria? Because although there are some that are really common causes of UTIs, urine infections, there are still nevertheless a number of different bacterial species that can do it, and they are quite different, some of them. So will this work to detect all of them and their sensitivities?
Oliver - Most urinary tract infections are caused by either E. coli or Klebsiella, but we also monitor the whole range of microorganisms to ensure this platform is accurate across not just one disease type, one just infection type, but multiple.
Chris - One of the things that the microbiology team in a lab will do is that they'll not just say which antibiotic works or not, they'll also give some indication of how sensitive the bugs are to it, so that doctors can make an informed choice. I'll go for the super sensitive one, or I'll go for one that's a bit more of a risk, but it's a lot cheaper. Can you do that too? Can you say we know how sensitive they are relative to each?
Oliver - Absolutely. So at the moment, for example, most of these tests are done by a method called disk diffusion. That requires you to measure with a ruler or a template the ring of growth or no growth around that little disc of antibiotic. We're able to simplify that all the way down and say for this given concentration of antibiotic, we see this growth from this, we see this amount of growth, and then categorise that and bring that back to a meaningful dose that the clinician can then take forward into their prescription.
Chris - And why stop with just urine? Could you do this for other things? Because micro labs are growing blood cultures, they're taking swabs from people's noses and throats and wounds and so on. Can the same thing not equally speed up those diagnostics?
Oliver - Absolutely. So we've chosen to start with urine. It's the most prevalent bacterial infection that's tested globally as a starting sample. Antibiotics are almost always given out for a urinary tract infection. And there's also up to a 60% rate of reinfection within UTI within six months. So how do we make a big impact on antimicrobial resistance as a whole antimicrobial usage? It starts there. But there's no reason why this technology can't be deployed and in the future will be deployed in things like blood swabs and joint fluids.
Chris - And the cost? Because at the end of the day, that is the thing that the accountants are going to look at. If it's saving them time, as well as saving money, it's a win-win.
Oliver - Yeah. So for us, this was really important from the get-go. And I said earlier that we called our platform Pragmatic Microfluidics. We've always wanted to make a platform that fitted directly within the workflow and was price competitive with that of a Petri dish. And so what we're really trying to do is to rapidise the routine here. So we bring rapid technology down to routine sample analysis. And when it makes it to market, it will be price competitive with the current workflow and what microbiologists already use.
Chris - And how far away is that?
Oliver - We spun Astratus out at the end of 2024 and we're moving down that regulatory roadmap. Unfortunately, with these technologies, or fortunately for these technologies, you can't just sell them. They have to go through a rigorous trial and regulatory procedure. And for us, that looks like 2028 by the time this will make it to market. And it will be deployed prior to that as a research use only tool and trying to build as much pilot traction and traction with laboratories up to that point, but it will be for sale by the start of 2028.
16:26 - How many childhood infections does daycare cause?
What is the burden of disease for babies and parents linked to nursery...
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How many childhood infections does daycare cause?
Sarah Caddy, Cornell University
Many would say, until you become a parent, you haven’t heard the half of it… because when children start nursery or daycare, it often feels like they’re ill all the time, and not just them, so are their parents! Runny noses, fevers, stomach bugs, you name it… one infection just seems to roll into the next. But what is the true scale and impact of this? And does it have to be like this? In a recent piece in Clinical Microbiology Reviews, vet, virologist,  and - crucially - parent Sarah Caddy, at Cornell University, wins Chris Smith's prize for -  in his view - the best titled manuscript this year with her analysis of children’s nursery infections entitled: “Germ factories, or immune boot camps”...
Sarah - So this was us having a conversation as a group of parents who are also virologists, immunologists and clinicians and trying to get to the bottom or understand why when our children started childcare, we were suddenly thrown so many challenges with them getting sick, followed by us getting sick and having to navigate that as parents with a career and trying to keep our employers happy at the same time.
Chris - You've called it germ factories or immune boot camps. Were you altogether surprised though, because we've known for a long time that if you put lots of little kids together, they don't understand the first thing about hygiene. They don't understand the first thing about Pasteur and germs. They just share everything. And I mean everything and that goes for germs. Is it really not that surprising?
Sarah - So I completely agree. I mean, from what we know biologically, this makes perfect sense. You know, these are germ factories and immune boot camps at the same time. And yet I remember my children first starting in childcare and being really surprised by this sudden influx of infectious diseases in our household. And so I think what we were hoping to do was to, I guess, make new parents and their employers aware that this is absolutely expected, this is normal and to sort of have management of expectations about what happens when you put your child into childcare.
Chris - Well, just summarise some of the key findings because you've reviewed a huge wealth of literature in compiling this report. So what are the sort of standout findings from this?
Sarah - So I think some of the most useful things we uncovered was the fact that we now have a clearer idea of how many infections you might expect over a year once your child is in a childcare setting. And so we expect up to two cases, possibly more, of diarrhoea and vomiting. You should anticipate a rash-forming disease once your infants pass one years old. And an astounding 12 respiratory infections can occur each year as well. And these may be as simple as a cold every month, but they can be more severe as well. So having that expectation that all these infections can occur, I think, is really important.
Chris - What about knock-on effects for parents? Did you get any instinct or insight into how many of those infant infections translate into an ill parent in the aftermath?
Sarah - Yes, and absolutely. There is quite a number of studies that have looked at this with diarrhoea and vomiting. If an infant has a case of diarrhoea and vomiting from an infectious cause, there is at least a 30% chance that's going to spread to another member of the household. And there was another study that showed if you do have an infant living in a household who's in out-of-home childcare, so essentially in a nursery, you are three times more likely to have acute gastroenteritis or that diarrhoea and vomiting over the year period than if you don't live with a small child.
Chris - And if you don't daycare your children, does this mean you get away with it? Or are we robbing Peter to pay Paul in the respect that they're going to have to catch this stuff at some point, because there aren't vaccines for all these things, for the majority of them are there. So does that mean that when they go to school, it's catch-up time and we just pay later?
Sarah - Children's immune responses are going to be completely naive. So by that means, they haven't seen these infections before when they first enter a setting with other children. And whether that is when they're 12 months old and in childcare, or whether it's when they're starting school, their immune response is going to have to rapidly develop to that infection. So if it doesn't happen earlier on, absolutely the child is going to encounter these infections later in life.
Chris - Do the data give us any insights into when it's best that this happens? From an immune development point of view, is it better for little kids to catch lots of stuff? Or does it not matter when we catch stuff, the immune response amounts to the same thing?
Sarah -  So that is a great question. And actually, it does depend a little bit on which virus or bacteria we're talking about. So for example, we know that with chickenpox, the risks associated with an infection, actually the risks are greater as the child gets older. So if you get chickenpox later in life, you're more likely to have more severe disease. But the converse is true of things like respiratory syncytial virus, or RSV, because an infant under 12 months old who's infected by RSV is going to get more severe disease than an older infant. So it's a balance. It's a hard one to navigate. But I think what we really wanted to get across from this review is to make people aware that there's going to be no perfect time for this to happen. But making sure that you're doing all you can to protect your infants in terms of vaccination, and ensuring good hygiene. These have got to be important ways for parents to protect their infants.
Chris - And any practical tips that you can volunteer? Having reviewed all this literature, and distilled out the numbers that you did, do any trends emerge where you think this is what I would do? This is definitely what I wouldn't?
Sarah - Absolutely. So I think it's really important to make sure that your infants are vaccinated against everything that is available. I think that's really key. And so for example, I'm really glad to see that the UK has now introduced the chickenpox vaccine for infants that are 12 months and older. I mean, a small anecdote is, yeah, my first child got chickenpox at 13 months old, and I took a week off work. And it was very stressful for everyone involved. But my second child, we went privately to get the chickenpox vaccine because I knew what the disease was like, and what the experience, emotional experience was as a parent. And so I'm really excited to see this, this now available and being rolled out across the UK. And I would strongly urge any parents to, to get every vaccine that they possibly can. But in terms of what age to put your child in I personally think risk of infection doesn't necessarily need to come into the equation. And there's so many other benefits to having child care for availability when needed. So I guess this is more of a story of reassuring parents and also raising awareness to employers about what to expect.
24:00 - Mega lasers: powering up lasers by orders of magnitude
The photonic equivalent of a sonic boom can dramatically increase laser amplitude...
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Mega lasers: powering up lasers by orders of magnitude
Robin Timmis, University of Oxford
A team of physicists have demonstrated for the first time a new way to dramatically boost the intensity of high-power laser light. They do it by firing an already very powerful laser beam at a material surface. So much energy is dumped rapidly into the surface that it turns into a state of matter called a plasma: essentially a fluid of charged particles. These then begin to resonate in lockstep with the laser, spitting out new pulses at extremely high energies. It’s the photonic equivalent of a sonic boom. The team hope that the findings - published in Nature - will lead to the most powerful lasers ever created, orders of magnitude more energetic than what we can make at the moment. Among other things, these will enable us to begin to probe problems and ask questions about the quantum realm that are beyond the reach of current physics. Speaking with Chris Smith, Robin Timmis did the experiments at the University of Oxford…
Robin - What we've done here is we've taken a really bright laser source and interacted it to be able to kind of boost the intensity of that light even further by many many times the original intensity that it was.
Chris - So it turns a super laser into a mega laser?
Robin - Pretty much, yeah!
Chris - How are you doing that?
Robin - We study this interaction where you take one of these lasers and you focus it down onto a solid target and when you do that you create this relativistic interaction so all of your matter in that target starts moving at the speed of light and that allows you to then get these really cool effects in the reflected light off that surface.
Chris - So it's a mirror that you're bouncing it off?
Robin - Yeah, yeah, you essentially turn your target into a mirror but then that mirror starts moving.
Chris - And why does the movement matter?
Robin - This is the whole key thing, right. This is something that probably a lot of people are familiar with. When you have an ambulance go past you and the sound changes coming from it as that fast moving object is either coming towards you or away from you, you get this change in frequency from the sound there. So, essentially, we're doing the exact same thing but now just with light where we get our mirror to move fast enough that it changes the frequency of the light that comes off it.
Chris - Is this sort of the light equivalent of a sonic boom then, in some respects, where all of the light sort of heaps up and you get a much more powerful effect?
Robin - Oh yeah, I like that idea, exactly! Yeah, starting with just something that was like a sine wave and then when you reflect it off you end up with these pulses of radiation. Each of them are very, very short in duration.
Chris - And how much more powerful does this make a laser then?
Robin - We are pretty optimistic about where this can go. People have suggested like if we can get this working properly 10,000 times intensity boost may be reasonable which is, you know, quite an exciting breakthrough considering at the moment we're sort of operating with high power lasers on just getting like an order of magnitude increase.
Chris - Does it work with all colours, in other words frequencies or wavelengths of light, or are you focusing on one particular wavelength at the moment?
Robin - Yes, that's something that's quite cool about this field is that it should be kind of scalable. We can do this with all sorts of different frequencies and we're looking at that in many different ways actually. But at the moment, yeah, we're focusing on infrared light.
Chris - And do you need a special mirror, in other words a solid surface that does the vibrating effect?
Robin - There are definitely some materials that are better than others but the kind of cool thing as well is you could probably do this with pretty much anything if you had the right sort of laser because you start with this solid and you're turning it into a plasma. The actual material doesn't matter so much when you do that.
Chris - When you say turning into a plasma, so does the surface that's being the mirror, does that effectively vaporise then in order to make this effect happen?
Robin - What you essentially do is you put enough energy in that all of the electrons that are in your atoms in that surface get ripped out. So you end up with this essentially a sort of liquid that's composed of charged particles.
Chris - And then they're seeing the laser light coming in and they're then doing the movement or the vibration effect that has this amplifying effect?
Robin - Yeah, exactly. It's the electrons, because they're the really light particles. They're the ones that actually start to accelerate to these very high speeds, almost to the speed of light, and can therefore all move around together coherently and create this mirror surface.
Chris - Why doesn't the mirror surface just completely evaporate instantly then? The minute you start putting all this energy in and you turn it into a plasma, why does it not just all evaporate? How do you confine that plasma where the laser light is incident so that you can actually get this effect for long enough for it to be useful?
Robin - You've actually hit the nail on the head there with that question about what's actually really interesting here and what we've managed to do. Essentially, you're completely right. That does happen, which is why you've got to hit these things really hard and really fast. If you don't hit your target hard enough and fast enough, then that's what happens. You eventually destroy it and you don't get this interaction at all, which is why you've got to operate with these very, very clean pulses that are very, very precisely tuned to enable this interaction to happen.
Chris - In the aftermath, does the surface stay intact? So in other words, could this be something that could be a sustainable process? If you can actually harness this, you wouldn't end up having to replace your mirror every time you fire a laser pulse.
Robin - This is the big problem with my entire field actually. These are very much single use situations. There's a lot of people working on ways of creating targets that will instead be regenerative in this way. But for now, yeah, you end up with a big damage mark on your pieces of glass.
Chris - What can we do with it though? Now you've discovered this, you've shown that hitting a surface really hard like this will produce these really interesting effects with this dramatic power increase. What can we do with it?
Robin - There's many possible things that we're looking into. For example, if you can get enough energy into a small enough volume of space, then you can start actually directly interacting that light with the vacuum and start to get all sorts of interesting quantum effects happening from that interaction. The thing is, you know, at the moment we are about a million times away in terms of light intensity from being able to do that. So at the moment it's just completely unfeasible for us to reach those levels. But maybe, maybe we could actually, you know, via this sort of technique, start to approach the desired intensities.
Chris - If you are able to do that and you get these quantum effects, well what can we do with them? Why is that useful?
Robin - So this application is very much just about testing theories we have about the fabric of the universe and essentially testing things that at the moment we can only do theoretically. So hopefully we'll reach a new sort of regime where we can do laboratory tests. That is the real physics, I think, once you can actually do the experiments.
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