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1:17

Hello? Claude, it's Ed Gamble.

1:19

Hi. Quick one. I've had an idea.

1:21

I want to do an official Traitors podcast

1:23

for the new series. Go on. Well, we've

1:25

got these amazing reactions of the banished players

1:27

when they find out who the Traitors actually

1:29

are. Yes, yes. Go on. Plus, I can

1:32

actually get them on the pod for their first

1:34

post-show interview. Ask them all about their experience in

1:36

the castle, who ate the most croissants at the

1:38

breakfast, all of that sort of stuff. This is

1:40

genius. I'm so sorry, but I've got a shepherd's

1:42

pie burning in the oven. I've got to go.

1:44

Keep me updated. Oh, OK. Bye, Claude. The

1:47

Traitors Uncloaked, the official companion podcast

1:49

with me, Ed Gamble. Listen on

1:51

BBC Sounds. Hello,

1:54

welcome to 5 Live Science. I'm

1:56

Chris Smith from the Naked Science Network. And

2:00

in the programme this week, what the structure of your

2:03

retina reveals about your risk of developing a range of

2:05

different diseases have we finally cracked

2:07

how the first biological cells appeared four

2:09

billion years ago and how

2:11

pond skater insects survived potentially lethal

2:14

run-ins with large raindrops. And

2:16

we're confident that maybe within the next five

2:19

to seven years, if we

2:21

can get these complement drugs into the

2:23

brain, we will have some therapies there

2:25

because these are already used for

2:28

other diseases. We're continuing our

2:30

Titans of Science series this

2:32

week, interviewing Wales's former chief

2:34

scientist and Alzheimer's guru, Julie

2:36

Williams. The Naked Scientists

2:38

on 5 Live. First

2:41

this week, a new study has found that

2:43

the structure of the retina at the back

2:45

of the eye can reveal a host of

2:47

diseases that a person is at risk of

2:49

developing. By using machine

2:51

learning to marry up changes seen

2:53

in retinal images with health and

2:55

genetic data taken from tens of

2:58

thousands of people who participated in

3:00

the UK's Biobank study, mass

3:02

IONA hospital ophthalmologists, Maryam Zekovat and

3:04

Nazli Zebedast think that they have

3:07

come up with a way of

3:09

using the retina to see what

3:11

a person's future health looks like.

3:14

In recent years, we have come to

3:16

realize that we can find out a

3:18

lot more information from images of the

3:20

eye than we ever thought was possible.

3:23

And it's opened up this really exciting

3:25

area of research. And

3:28

we were fortunate enough to

3:30

have access to an incredible

3:32

resource, specifically a large, large

3:34

study of about half a million people

3:37

from the UK called the UK

3:39

Biobank. And we had

3:41

images of people's eyes. And we

3:43

were wondering, is there a link

3:46

between images of the eyes? And

3:48

Maryam, we'll talk a little bit

3:50

more about how those were obtained

3:53

and our killer and systemic disease.

3:57

Maryam, what are these pictures you've got of

3:59

people's eyes? looking at the outside or

4:01

are you talking about what's going on

4:03

inside the eye? It's

4:06

inside the eye that human

4:08

retina is a multi-layered tissue

4:10

which offers a really unique

4:12

window into systemic health. So

4:14

here we're looking specifically at

4:16

that retina which is composed

4:18

of nine different layers using

4:21

OCT imaging, optical appearance, tomography

4:23

imaging and that's a non-invasive

4:25

imaging that uses light waves

4:27

to take a cross-section picture

4:30

of your retina. And

4:32

so we have this OCT imaging available

4:35

across 50,000 individuals

4:38

in this biobank. And

4:41

Nazli, why should looking

4:43

at the different layers of the retina

4:45

give us an insight into a person's

4:47

overall health or disease risk? Some

4:50

of it is actually really surprising. So

4:52

for example, we didn't know before the

4:55

machine learning models came out that we

4:57

could tell someone's age just by

4:59

looking inside their eye or

5:01

their sex even. But

5:04

what is, you know, the retina is a

5:06

very intricate tissue. It's

5:08

an extension of your brain essentially.

5:11

And so it's constructed of all these

5:13

different cell layers that are connected to

5:15

our brain and our systemic health or

5:17

essentially your overall health. So

5:19

you can look at people's eyes and

5:22

when they say the eye of the window into

5:25

your soul, they're not really kidding because

5:27

you're seeing what is

5:29

going on with someone's heart, someone's

5:31

blood pressure potentially, even

5:34

how they're breathing or their

5:36

risk of having certain neurologic

5:38

problems. And Maryam,

5:40

when you did this study, what

5:42

did you actually measure and what did you marry

5:45

up with what? So what

5:47

we measured was the thickness of each

5:49

of these nine layers of the retina.

5:51

And we used this measurement to then

5:54

look at connections to systemic

5:56

health to disease and also

5:58

to genetics. Nazli,

6:01

one of the key things about any kind

6:03

of disease, we always say prevention is better

6:05

than cure. So the critical question

6:07

I can ask you is, if you do this, does

6:10

it give you a window into the

6:12

early stages of a disease at a

6:14

time when you might be able to

6:16

intervene meaningfully in a person before they

6:18

actually get sick from something? It's

6:22

interesting that you asked that. One

6:24

of the key pieces of analysis

6:26

that we did in this manuscript

6:29

was looking at future

6:31

risk of disease. So looking

6:33

at someone's retinal thickness and

6:36

determining if that was linked

6:38

to future disease

6:40

diagnosis. And in

6:42

fact, the layer thicknesses of

6:45

the retina are predictive of

6:47

future diseases of the

6:49

heart, of the brain, of the

6:51

kidneys, of the lungs, including eye diseases

6:54

as well. So even

6:56

though this needs to be confirmed,

6:58

our study does point to the

7:00

fact that we can use retinal

7:03

thicknesses or retinal phenotypes to be

7:06

able to predict disease before it

7:08

happens and intervene. So

7:11

would the approach be then that rather

7:13

than subjecting a person to a whole

7:15

raft of different tests and blood samples

7:18

and genetic analyses, you could plonk them

7:20

down in front of you, use

7:23

this technique to look at their retinal

7:25

structure, and then based on

7:27

what you've learned about the associations between

7:29

the different shapes and structures of the

7:31

retina and different disease outcomes, you could

7:34

make predictions about what a person might

7:36

be about to develop or indeed

7:39

is developing right now, and

7:41

then you can make obviously interventions

7:44

as necessary. Precisely. I

7:46

think that is exactly how

7:48

we envision results like this

7:50

being used. As

7:53

Maryam previously mentioned, also the

7:55

OCT or these light pictures

7:57

of the eye are routinely

8:00

used in clinical practice and ophthalmology.

8:02

And so, you can imagine if someone comes

8:05

in for their eye exam, then you can

8:07

use this information to tell them you seem

8:09

to have a high risk of MS or

8:12

you have a high risk of high

8:14

blood pressure or you might have

8:16

a high risk of developing diabetes.

8:18

So you should go see your

8:20

primary care doctor. The other

8:22

way you can think about this is exactly as

8:24

you said is what if we

8:26

just had this as a screening, a

8:30

tool where people would come in, get

8:32

images of their retina noninvasively without having

8:34

to do all these extra tests. And

8:37

they could know that they have risk for

8:39

certain diseases that they need to get checked

8:41

for or even treat us for

8:43

potentially. Nasely Zebedast

8:45

and before her, Mariam Zekovat there, they

8:47

published that study in the journal Science

8:49

Translational Medicine. The

8:52

origin of life on earth and beyond

8:54

is a mystery and arguably

8:56

one of the most important questions that

8:59

we need to answer. We

9:01

know that life started simply, probably

9:03

with self-replicating chemical reactions, most likely

9:05

based around something similar to the

9:07

DNA molecules that we rely on

9:09

to carry our genetic code today.

9:12

But pretty quickly, those reactions found

9:14

a way to wrap themselves up

9:16

inside oily membranes that could protect

9:18

them from the surroundings and make

9:20

the process more reliable and efficient.

9:23

Hey, presto, the cell was born. But

9:26

where did those membranes made of fatty acids

9:28

come from in the first place? That

9:31

question has bothered biologists for decades. Now

9:34

though, researchers at Newcastle University

9:36

have recreated in the lab

9:38

the conditions around hydrothermal vents,

9:40

also known as underwater black

9:42

smokers. These conditions, John

9:44

Telling has found, can spontaneously generate

9:47

the very molecules of fatty acids

9:49

the scientists have been looking for.

9:53

There's a few lines of evidence that

9:55

point towards these hydrothermal vents, these hot

9:57

springs, as a... likely

10:00

place for where life originated. People

10:03

have tried to find out what the

10:05

earliest cell that everything originates from was

10:07

like. And what they've deduced from looking

10:09

at the genes is that the first

10:11

cell, known as the last universal common

10:13

ancestor, liked it hot. It

10:15

probably lived off of hydrogen gas. And it

10:18

would have used carbon dioxide as well to

10:20

kind of build itself. So those lines of

10:22

evidence all point towards these hot springs as

10:24

a possible place for the origin of life.

10:27

It sounds like we actually know quite a bit

10:29

in terms of what we expect that ancestor to

10:31

have been like. But what was the outstanding question

10:33

you were trying to crack with

10:35

relation to it then? Previous

10:37

people have tried running different experiments to

10:40

try and mimic some of the conditions

10:42

that these hydrothermal vents would have had.

10:45

People had either tried to recreate,

10:47

say, the high temperatures or the high

10:49

pressure or the kind of continuous

10:51

flow where you're mixing seawater with this

10:54

hotter fluid. But nobody had really

10:56

gone on to try and combine all of

10:58

those at once. So that's what

11:01

we wanted to do. So we built some new apparatus

11:03

and allowed to try and get that,

11:05

get the high pressure, get the high temperature,

11:07

and get the continuous flow all

11:09

in one experiment and try and react this

11:11

hydrogen gas and this carbon dioxide over these

11:14

metals to see if we could generate organic

11:16

molecules. What sorts of molecules

11:18

were you looking for? Those

11:20

we were particularly interested in were

11:22

these molecules known as fatty acids.

11:24

They have a fatty end

11:27

and a water loving end. The interesting thing

11:29

about them is if they get enough of

11:31

them in that water, then they can form

11:33

these what's known as called a membrane structure,

11:36

these vesicles or liposomes sometimes they're known as.

11:38

But they basically form these little round balls

11:41

surrounded by a membrane which separates what's

11:43

in them from what's outside.

11:45

So it's acting in a way as

11:47

a first cell membrane potentially, which could

11:50

be separate the external environment from the

11:52

internal and let different chemistry happen. I

11:55

understand where you're going with that because obviously that was

11:57

the big question wasn't it? If life gets started as

11:59

a... of chemical reactions, where did cells

12:01

come from? So if you've got a reaction that

12:03

can produce the oily bags that surround all our

12:06

cells, that is 90% of the equation. Well

12:10

it's certainly a good step forward. Yeah,

12:12

I mean it's the first step to

12:14

creating a self, yeah, something different from

12:16

what's outside. So the ability to do

12:18

that and then concentrate other chemicals differently

12:21

to outside, generate different reactions would be,

12:23

I think, an essential step for how

12:25

life started. So what are

12:27

the raw materials that you're feeding into your

12:29

pretend hydrothermal vent? And what

12:31

chemicals did you see coming out at

12:33

the end in these conditions that leads

12:35

you to think that is possibly how

12:37

some primitive cell light structures could have

12:40

formed? So what we fed in,

12:43

the basis of it was hydrogen gas,

12:45

which we added under pressure. And then

12:47

we combined that with dissolved carbon dioxide.

12:49

We're reacting them over a mineral, in

12:52

this case an iron-rich mineral known as

12:54

magnetite, to form hydrocarbons, organic molecules. And

12:56

in particular we were looking for these

12:58

fatty, ethane molecules, which are a type

13:00

of hydrocarbon. And do you get

13:03

many and how quickly? The experiments

13:05

we run so far, we only ran

13:07

for 16 hours. And in that time,

13:09

yeah, we generated enough to find them.

13:12

So we don't know. If we run it

13:14

for longer, we might find that we generate

13:16

even more of them. But there are certainly

13:18

enough of these organic molecules for us to

13:20

analyze. So they start

13:22

to self-assemble, because the point you're making

13:24

is that the fatty bits love other fatty

13:26

bits, so they tend to get together.

13:28

So do you start to see that happening?

13:32

As yet, no, because when

13:34

they form, they actually form on the mineral

13:36

surface. The next stage of experience that we

13:39

want to do is to try and do

13:41

this, to actually change the chemical conditions. We

13:43

think that maybe if we make the environment more

13:45

alkaline, we can get some of these molecules, particularly

13:47

these fatty acids, to lift off.

13:50

And hopefully we can then see them self-assemble.

13:53

So if we bring what you

13:55

found to the party that already people

13:57

had envisaged as to how life

13:59

could have gone, started. How do you bring

14:01

and unite your discovery of how these

14:03

fatty acids begin to form with

14:06

what people thought might also be going on around

14:09

the same time about 4 billion years ago that

14:11

was the start of life? People

14:14

have found these reactions going on at

14:17

higher temperatures, for example, before. What we've

14:19

done is do these experiments under more

14:22

realistic conditions as to what the conditions

14:24

may have been like on the early

14:26

Earth. And it just gives that greater

14:28

likelihood, I think, that these really important

14:31

organic molecules may well have been formed

14:33

within these sub-ocean hydrothermal vents. And it

14:35

might also increase our understanding as

14:37

well, I think, on about how life may

14:40

have originated in other places in our solar

14:42

system where a similar chemistry might be going

14:44

on. I was going to ask you about

14:46

that because, of course, we've got missions

14:48

that are going to be looking at

14:50

Europa, which is one of Jupiter's moons.

14:53

People have also considered Enceladus, one

14:55

of Saturn's moons, which appear to

14:57

have warm liquid oceans beneath the

14:59

surface of ice.

15:01

So it's possible the conditions there might

15:04

be similar to the conditions you're mimicking

15:06

in your laboratory. Exactly

15:08

so, yes. I mean, I think the

15:10

best characterised ocean so far is actually

15:12

Saturn's moon Enceladus. That's your

15:14

spacecraft, which has travelled around

15:16

known as Cassini. And it's actually sampled these

15:18

plumes, which people think are emanating from beneath

15:21

the kind of icy layer of Enceladus into

15:24

this ocean. So you've got part of this

15:26

ocean actually being blasted out into space and

15:28

then analysed. And when they've

15:30

analysed the sort of vapours and

15:32

particles that are in this plume,

15:34

they found hydrogen gas, they found

15:36

carbonate, so signs that carbon

15:38

dioxide is there as well. And they've also

15:41

analysed different organic molecules. It seems that all

15:43

the ingredients potentially for an origin of life

15:45

might be there, but it's going to take

15:47

a fair few more experiments to try and

15:49

narrow that down further. Absolutely

15:51

fascinating findings. Newcastle University's John Telling

15:54

there, and that paper's just come

15:56

out in the journal Nature Communications,

15:58

Earth and Environment. This

16:01

is 5 Live Science with me Chris

16:03

Smith. On the way, how do pond

16:05

skaters, tiny insects, survive being hit by

16:07

huge water droplets and later on titans

16:10

of science? I'm chatting to

16:12

Alzheimer genetics expert Julie Williams.

16:16

Well back to medicine and health now,

16:18

and Sarah Ferguson, the Duchess of York,

16:20

has revealed that she's been diagnosed with

16:23

malignant melanoma. The 64 year

16:25

old author and former high profile member of

16:27

the Royal Family said she was grateful for

16:29

the love and support that she's received and

16:31

has urged people to look out for signs

16:33

of potentially cancerous moles themselves. To

16:36

tell us more about the science and medicine

16:38

of malignant melanoma, here's Rhys James. Malignant

16:41

melanoma affects more than 300,000 people

16:44

around the world each year, and its

16:46

ability to metastasise or spread to other

16:48

parts of the body can make it

16:51

particularly pernicious. The disease accounts for

16:53

only 4% of all skin cancers,

16:55

but is responsible for 75% of

16:58

deaths caused by these malignancies. Melanoma

17:00

UK says your chance of surviving it

17:02

largely depends on how early it's caught,

17:05

and if it doesn't spread to your

17:07

lymph nodes or another part of your

17:09

body, then it's highly likely that simply

17:11

removing it will cure you. So

17:13

what should we know about how it develops in the

17:15

first place? Melanoma is caused

17:17

by ultraviolet light, and in particular

17:19

UVB rays from the sun and

17:21

also sun tanning beds. The

17:24

light damages the DNA melanin-producing cells in

17:26

the deepest layers of our skin. This

17:29

stops the cells repairing their DNA

17:31

from further damage, and locks

17:33

them into an uncontrolled growth cycle. Although

17:36

melanoma cases have roughly doubled since the

17:39

1990s, some of us are at greater risk than

17:41

others. People with fair

17:44

skin, fair hair and freckles are

17:46

particularly susceptible, as are those with

17:48

a history of the disease and their immediate family. Intense

17:51

and intermittent sun exposure, including frequent

17:53

sunburn, is associated with the greatest

17:56

risk. The average age for diagnosis

17:58

is 66. but

18:00

it is not uncommon for people in their 30s

18:02

to develop it. Thankfully, greater

18:05

awareness has led to a reduction in

18:07

the number of children dying from melanoma

18:09

in recent years. This has

18:11

been in no small part due to successful

18:13

health campaigns run around the world, included

18:16

in Australia and New Zealand, which have

18:18

the highest global rates of melanoma. The

18:20

famous Slip Slop Slap campaign in the

18:23

1980s, which featured Sid the Seagull encouraging

18:26

people to slip on a shirt, slop

18:28

on the sunscreen and slap on

18:30

a hat, remains great advice to

18:32

reduce and avoid sun exposure. So

18:35

what should we be looking out for if we think

18:37

something isn't quite right? Sarah Ferguson

18:39

said her melanoma was discovered following the

18:41

removal of what turned out to be

18:44

a cancerous mould during treatment for breast

18:46

cancer. The NHS advice

18:48

here in the UK says that in

18:50

order to catch the disease as early

18:52

as possible, we should all be looking

18:54

out for new moulds, a change in

18:56

an existing mould, large moulds and even

18:58

moulds that are either uneven in shape

19:00

or a mixture of colours, and

19:02

especially those that are particularly dark, itchy

19:05

or tend to bleed. If

19:07

melanoma is caught early, it is likely

19:09

that it will not cause further problems.

19:11

The first step in treatment is usually

19:14

surgery to remove the affected area and

19:16

check that it has been completely excised.

19:19

This is curative in the majority of cases,

19:21

but some people will present with disease

19:24

that has already spread from the primary

19:26

sites or return with a relapse later,

19:28

in which case patients are treated with

19:30

chemo or immunotherapy. Professor Sarah

19:32

Allinson has written a great piece

19:34

in the conversation about the huge

19:36

improvements in treatment over the past

19:38

decade, including the development of drugs

19:40

such as dabra-phenib or tremetinib.

19:43

These new agents prevent cancerous cells from

19:45

growing and also allow the immune system

19:47

to recognise them as hostile and destroy

19:50

them. Some patients have now

19:52

been cured with these therapies, despite presenting

19:54

with extensive disease, proving that they can

19:57

work in some cases. Now

19:59

the race is on. to work out how to

20:01

make the process effective for everyone. Nevertheless,

20:03

when it comes to cancer, prevention

20:05

is, of course, always better than

20:07

cure. So be sure to

20:10

remember the advice of Sid the Seagull, and

20:12

slip on a shirt, slop on the sunscreen

20:14

and slap on a hat. And if you

20:16

notice that you have new moles, a change

20:18

in an existing mole or large moles, then

20:20

speak to your doctor and get yourself checked

20:22

out as soon as possible. Well

20:25

nature now, and researchers in the United

20:27

States have made a big splash in

20:29

the science field this week by using

20:31

ultra-fast photography to watch what happens when

20:33

pond skaters, called water striders in

20:35

America, are hit by falling

20:37

raindrops which massively outweigh the tiny

20:39

insects themselves. For them, it's

20:42

like one of us standing under Niagara

20:44

Falls. Also, says the study's author at

20:46

Florida Polytechnic University, Darren Watson.

20:50

We did this by first capturing

20:52

the insects from our local ponds,

20:55

and we had to create a

20:57

rainfall simulator. So we had

20:59

a reservoir of water that we

21:02

pumped through a nozzle that

21:04

mimicked raindrops. Those raindrops

21:06

struck the insects, and we observed

21:08

the interaction using our high-speed video

21:11

cameras in the lab. So

21:13

you go in the shower, basically. How

21:16

fast is fast? When you say high-speed

21:19

imaging, how many pictures a second are you

21:21

taking of this? We can

21:23

capture up to 4,000 frames per second. So

21:26

it's very fast. We see the

21:29

droplets move in on the order

21:31

of milliseconds. Talk

21:33

us through them. When you look at this footage, what

21:36

does it show? Before

21:38

we talk about what occurs with the

21:40

insects, when a raindrop

21:42

hits a pool of

21:44

water, what you're going to get is a

21:46

splash. And we are all familiar with splash.

21:48

We see this during rainfall. But

21:51

that splash constitutes a

21:53

couple different phases. So we see

21:55

an underwater crater. We

21:57

see a jet that goes back up. above

22:00

the water surface and it was

22:02

important for us to look at

22:04

how the insect interacts with these

22:07

different components of the splash. So

22:11

when the insect is struck by

22:13

a raindrop, we see that the

22:15

raindrop pushes the insect into the

22:17

water body and the insect

22:19

you'll find that along the

22:22

the inner surface of

22:25

that particular raindrop as it creates

22:27

a crater inside the body of

22:29

the water. So we find that

22:32

the insect is you can

22:34

see attached to the to the water at

22:37

that point in time. So then

22:39

when the jet is formed it is transported

22:43

out of the water with

22:45

the jet. So

22:47

the water gets pushed downwards

22:50

and outwards and compressed

22:52

by the incoming droplet and what is

22:54

it a rebound of the water coming

22:57

back in underneath the insect that creates

22:59

a jet like almost like a geyser

23:01

underneath it that pushes it up in the air. Yes

23:04

the rebound occurs as the dented

23:06

surface of the water tries to

23:08

go back to its original state.

23:11

So raindrop pushes the

23:13

insect beneath the water

23:15

and then there's a rebound

23:17

and you have the jet coming

23:20

upwards. Does the

23:22

action stop there or do do

23:25

you then get secondary effects because obviously what goes

23:27

up must come down if you made a jet.

23:30

Do you then get secondary rain

23:32

effectively off the back of having hit the

23:34

insect the first time? Yes

23:37

and that is where the danger

23:39

lies for the infant because that

23:42

jet then disintegrates to create what

23:44

you would have termed secondary rain

23:47

and it then pushes

23:50

the insect inside the body of the

23:52

water again and we find

23:54

that the rebound is going to

23:56

be so precipitous That the insect

23:58

is going to be left. Beneath.

24:01

The waterline. Does

24:03

it have to swim up And then how

24:05

does it break through? Assuming it does the

24:07

surface of the water because the surface tension

24:10

there. Between. the air in the

24:12

water isn't there so had seen sick get

24:14

back through their an end up on the

24:16

s I'd. Rather than on the

24:18

waterside, This. Is rather

24:21

he needs to the infant

24:23

because insects are generally boring

24:25

beneath. The water line. And.

24:28

The young's what they do. You

24:31

swim to the top I'm to

24:33

wear that waterline is and be

24:35

break. The. Surface to get onto

24:37

the air sites. all the others are awful

24:39

him to do that and they do that

24:41

through a series of. What? We

24:44

call Power Strokes. Applied at

24:46

an acute angle and that allows

24:48

the insects to be able to

24:50

break that water line to get

24:52

back on through the air. Side

24:54

of things. There. Was doing quite

24:56

well because there's loads of them and if

24:58

I look at the pond near where I

25:01

live there's there's many many to council. Dorsey

25:03

pretty good at this is by She with

25:05

the terrible. Whether we have spits, what are

25:07

the applications of this? Because it's It's interesting

25:10

in a fascinating to understand how these insects

25:12

have evolved to have this behavior. but understanding

25:14

this now as you do can you apply

25:16

it to any other aspects of what we

25:18

see in the marine or aquatic realm? Yes,

25:21

Weekend on ourselves here. They

25:24

will allow us to better

25:26

understand the transport of floating

25:28

particles like macro plastics on

25:31

the earth. Water bodies know

25:33

micro plastics are similar in

25:36

size to our water strider

25:38

or in your case on

25:40

skaters, and they would likely

25:43

share a similar experience during

25:45

rainfall. Act. As

25:47

a matter of fact, in some of

25:49

our experiments, we replaced what as traitors.

25:52

With. sorting particles and observe

25:54

be similar interactions so that's

25:56

the mean real our application

25:58

of the study at moment and

26:00

we're going to be seeking to Darren

26:08

Watson there, he's just published that study in

26:10

the journal PNAS. Ryan

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the next half an hour, we're continuing

27:55

our Titans of Science series. The

27:57

Naked Scientists on 5 Live. Julie

28:01

Williams was born on the 11th of September

28:03

in 1957 in Murtha, Tydfil in Wales. Julie

28:08

attended the Scolly Greg Primary

28:10

School and Vayner & Penderan

28:12

Comprehensive School before she studied

28:14

psychology at the University of

28:16

Cardiff. Professor Williams is a

28:18

leading authority on neuropsychological genetics

28:20

and her research aims to

28:22

study the risk of developing

28:24

psychological and neurodegenerative disorders like

28:27

Alzheimer's disease. Julie also served as

28:29

the Chief Scientific Advisor to the Welsh Government

28:31

between 2013 and 2017. She

28:35

was just the second person to hold down that

28:37

job. She's currently the

28:39

Centre Director at the UK Dementia

28:42

Research Institute in Cardiff and in

28:44

her spare time she enjoys relaxing

28:46

with her family and

28:48

she watches rugby. Alzheimer's

28:50

has dominated your professional

28:53

career. But what actually is

28:55

that? When we say that word, what do we

28:57

mean? Well I think most

29:00

people are familiar with memory problems

29:02

that occur usually late

29:04

in life and those develop

29:06

into a full-blown degenerative

29:08

disorder that is terminal. But

29:11

actually Alzheimer's begins probably about

29:14

20 years before that, so

29:16

it's asymptomatic in its early

29:18

stages. And why did you

29:20

end up going down that path? I

29:22

was interested initially in how the brain

29:25

worked and that got me into psychology.

29:27

But I was a little frustrated with

29:29

not being able to understand it at

29:31

a level that I wanted

29:33

to. So when the opportunity arose

29:36

to go into something more

29:38

biological and specifically genetics, I

29:40

took it. And that has opened up a

29:43

greater understanding of the sort

29:45

of minute processes that go

29:47

to diseases

29:50

such as Alzheimer's disease. So

29:53

when back in history did you actually

29:55

start working on the disorder? Gosh it's

29:57

probably about 25, 30 years. years

30:00

ago I would say. I joined

30:02

a team headed by Peter

30:04

McGuffin and really

30:06

just went from there. It's

30:08

an amazing area, genetics. It

30:11

seemed to develop new ideas, new

30:13

methodologies, almost every year we were

30:15

able to do a lot more.

30:17

So it was a very

30:20

exciting area but it opened

30:22

up our understanding of the

30:24

biology underlying these diseases. Let's

30:27

go back a bit further

30:29

than the start of your career

30:31

because Alzheimer's disease is named after

30:34

Alois Alzheimer who was a French

30:36

neurologist slash pathologist. He

30:39

recognised this disorder in its first

30:41

instance. What would he have been

30:44

looking at? He would

30:46

be looking at individuals that presented

30:48

and the first individual that presented

30:51

with a degenerative dementia

30:54

and he took that through

30:56

to after death of this

30:58

individual to look at the neuropathology. He

31:01

was described the neuropathology

31:03

in great detail drawing out

31:05

what he saw in the

31:07

brain of this individual and

31:09

subsequently others. You

31:11

saw clamps of amyloid plaques, these

31:14

plaques that were found outside

31:16

the neurons, the brain cells. There

31:19

were rectangles within neurons and

31:22

there was a lot of immune

31:25

activity that the glial cells were

31:27

also in his drawings,

31:29

actually there were drawings of

31:31

glial cells than neurons. So

31:33

he was trying to describe and understand what

31:36

the picture was and identifying

31:38

this as a genuine disease, not

31:40

really a natural way

31:43

of aging. How had that

31:45

picture changed about 100 years later

31:47

when you embarked on your

31:49

work? At the time we

31:51

knew through studies of twin studies that

31:54

genes were playing a significant role

31:57

in Alzheimer's disease, we knew

32:00

that those with very early

32:02

onset disease had

32:04

more of a genetic contribution.

32:06

Early onset Alzheimer's before the age of

32:08

65, you have

32:11

about a 90% heritability based on

32:13

these studies. And we knew that

32:15

were certain families that had

32:17

a very strong risk of

32:20

getting Alzheimer's. So there were mutations.

32:22

At the time, we knew these

32:24

mutations. If you had some

32:27

of these mutations in the genes at

32:29

the initial status and then at that group

32:31

of three, you would get

32:33

the disease. And we could always predict

32:35

within five years when you would develop

32:37

those disease. But these were extremely rare,

32:39

these families in the population.

32:42

So we knew genes were there to play

32:44

a role, but we didn't know what they

32:47

were for the majority of

32:49

cases. So that was

32:51

to become the major target for your

32:53

life's work, as it were. Let's

32:56

wind back before we talk about that a bit

32:58

and consider how you got to the stage where

33:00

you could even take that on. I mentioned where

33:02

you went to school, but were you

33:04

from a sciencey family? No, not

33:07

really. My father was a businessman. My mother did

33:09

a lot of charity work. But

33:11

my father was always curious. And

33:13

we routinely sit down

33:15

to watch Tomorrow's World. And

33:18

he'd always encourage us to do

33:20

new things and try out new

33:22

activities or new experiences. So we

33:25

had an upbringing that

33:27

allowed us to think more and

33:29

become curious. My sister is also

33:31

a pharmacist. And she went

33:33

into science in a different way. So

33:35

it affected us. So you

33:37

had that, I suppose, springboard into

33:40

the area of interest. But having

33:42

the interest and then translating into

33:44

being a professional, that takes a

33:46

bit more, doesn't it? So what was it that made

33:48

you say, no, I'm actually going to do this? Well,

33:51

I suppose there were other influences. Well, one

33:53

of the things that really influenced me was

33:55

this series called The Ascent of Man by

33:57

Brinovsky. And I've started to rewatch it actually.

33:59

because it's come back on. And this is

34:02

about somebody who is curious about

34:04

a variety of things, but it was the

34:06

science and the biology that really intrigued

34:09

me. And as I then

34:11

went on to do my degree, trying

34:13

to understand how the

34:15

brain worked, people like Broadbent influenced

34:18

me because he was trying

34:20

to understand the brain in a very

34:22

conceptual way, but it was limited. And

34:24

I remember reading something he wrote

34:27

about the frustration that he

34:30

would probably never see in

34:32

his lifetime this biological basis

34:34

to cognition. But I

34:36

thought, well, it would be rather nice to see some

34:38

of that in my lifetime. The problem

34:40

is that the situation you arrived at

34:42

where you wanted to grapple with the

34:44

genetics of this very important and very

34:47

common condition, but there

34:49

weren't the tools there when you started

34:51

that we really very much take for

34:53

granted today to do genetic work. When

34:55

we want to find genes, today it's

34:57

very, very easy in comparison to the

35:00

situation in which you would have found

35:02

yourself 30, 40 years ago. That

35:04

is true. And I've never been in an area where

35:07

we were learning new methods,

35:09

technologies, perspectives, almost on an

35:12

annual basis. So

35:14

yes, when we started, we would spend perhaps

35:16

nine months trying to understand a bit of

35:18

a gene to try and

35:21

describe its variation and compare

35:23

it between people who had

35:25

Alzheimer's and people who didn't.

35:27

Now we can do whole

35:29

genomes in a very short period

35:31

of time and really

35:34

interrogate those differences between those with

35:36

the disease and those without. And

35:39

what we also needed was to have

35:41

very powerful samples. That was another thing

35:44

that allowed us to find

35:46

these things out because there's a lot of

35:48

variation in there and you could be finding

35:50

things by chance a lot of

35:52

the time. So you need to build the power. And

35:54

that's what took a lot of time in

35:57

collecting enough people with a lot of

35:59

data. Alzheimer's comparing them to

36:01

people without. How did

36:03

you go about that then? So

36:05

you recruit families who have

36:08

a premature onset of Alzheimer's or

36:10

just lots of people who get

36:12

it. What were you selecting? And

36:14

then how were you trying to find out what

36:16

genes might be involved? Because in a genome of

36:18

20,000 genes, which we

36:20

now know, there are in a human,

36:22

that's a huge number of moving parts.

36:25

My interest was in understanding the

36:27

common forms of Alzheimer's disease. So

36:29

that was the initial focus, was

36:32

to collect hundreds

36:34

of people that we

36:36

could just sample their DNA through a blood

36:38

test or a saliva test and

36:40

describe their disorder. That

36:43

took a lot of time. But

36:46

we spent about 20 years collecting

36:48

throughout the UK, Northern Ireland, these

36:50

samples, and more lately, collecting rarer

36:53

samples of people with very

36:56

early onset disease, which

36:58

is more severe and probably more genetic

37:01

in its basis. But there's

37:03

going to be hundreds of

37:05

genes, thousands possibly, that could

37:07

influence the disease. And

37:09

how does one connect a gene that

37:11

someone carries to a disease? How do

37:14

you then square that circle

37:16

so you can understand what its contribution

37:18

is? So we would take individuals'

37:21

DNA. And the DNA has

37:23

markers throughout it that

37:26

can tell you whether there

37:29

is a variant that is

37:31

actually that variant or something

37:33

very close by to that

37:35

variant that is associated with

37:37

the disease. So we would

37:39

compare DNA from individuals with

37:41

Alzheimer's and without Alzheimer's. And

37:44

we would look at simple changes

37:46

that can occur in one

37:48

or two forms. These SNPs

37:50

are single nucleotide polymorphisms. And

37:53

if, for example, people without Alzheimer's

37:56

had more of the first sort

37:58

of that, than

38:00

those without, we could say

38:02

with some confidence that there was something

38:05

in that region that was associated with

38:07

Alzheimer's disease. It may not be that

38:10

particular SNP, but it may be something

38:12

close by to that. So it's

38:14

like a signpost that says in this

38:16

region of the genome there is something

38:19

linked to this disease and if you

38:21

have that particular marker then

38:23

probably in that bit of the genome

38:25

you have something that's going

38:27

to increase or decrease your chance of getting

38:29

that particular condition. So look at enough people,

38:32

enough times, with enough outcomes and you will

38:34

begin to home in on what those areas

38:36

are, even though you don't have to know

38:39

exactly what the gene is yet. That's

38:41

true. So what we were seeing

38:44

were patterns actually that were

38:46

quite surprising. When we

38:48

first did our initial very large, what

38:50

we called genome-wide association studies,

38:52

these are these big studies of all

38:54

the variants that tag

38:56

most of the genome, we

38:59

were seeing patterns that implicated our

39:02

immune system. Now that we

39:05

knew from Alzheimer's first drawings

39:07

that glial cells, immune

39:09

cells were there

39:11

around the damage in the

39:13

brains, but we'd always thought that this was

39:15

just a normal reaction to

39:17

something going wrong in the brain. But

39:20

what the genetics was telling us is these

39:23

changes in the immune system are

39:25

actually part of the pathway to

39:27

disease. If you look at

39:30

people who have Down syndrome, who have an extra copy

39:32

of chromosome 21, they

39:34

also get an Alzheimer's like

39:36

change in their brain, don't

39:38

they? So is the same thing going on or

39:41

is that a red herring? That's

39:43

a very good question. I think

39:45

there are a number of components

39:47

to this complex disease and the

39:50

component that is probably implicated

39:53

there is more to do

39:55

with the amyloid pathway if

39:57

you like and that's maybe what is

39:59

common. But it's not

40:01

exactly the same as as

40:03

common Alzheimer's disease, which is

40:05

contributed to by a number

40:07

of different components going

40:10

wrong at the same time. You

40:12

know, it's the accumulation of

40:14

risk in those various areas

40:17

that pushes you into a disease

40:19

process. So there are lots

40:21

of different factors happening at once. It's

40:23

not just that there's one cause, although

40:25

there might be in some people, I

40:28

suppose, but you've got lots of different

40:30

factors all playing a relative contribution. So

40:33

how can you unpick then which ones

40:35

really matter? The secret is to

40:37

try and use the genetics now as

40:39

a sort of platform to

40:42

then understand the biology. So

40:44

we look at individuals that have

40:47

some of the risk factors that are involved.

40:49

So we are now creating stem

40:52

cells that reflect

40:54

the risk in those individuals.

40:57

We also look at particular cells that

40:59

we know express a lot of the

41:01

risk factors. And one of these

41:04

cells is called a microglia. This

41:06

is a cell that has housekeeping

41:08

properties. It sort of has its

41:10

own little patch of brain that

41:13

it monitors and keeps clear of

41:15

toxins or bad tissue.

41:18

And what we know from the

41:20

genetics is that a lot of the

41:22

genes that we have found as

41:24

risk factors are expressed in microglia, some

41:27

solely in microglia. So

41:29

that's a big clue that they are

41:31

playing a significant role in part of

41:33

the pathway to Alzheimer's disease. So

41:35

does this mean then that chiefly this is a genetic

41:39

disease, Alzheimer's? No.

41:41

Genes play a role. We look at

41:43

these on a population basis, on

41:46

an individual basis. And

41:48

one individual may have a very

41:50

strong genetic contribution. Another

41:53

individual may have a more

41:55

environmental contribution. So now

41:57

we need to get down to the precision

41:59

medicine. a focus where

42:02

we can identify people that have

42:04

certain risks, certain

42:06

susceptibilities and we

42:08

may have different treatments or

42:10

preventions that are focused on

42:12

these individuals in the future compared

42:14

to others. How many genes then

42:16

do you now know that strongly

42:19

influence your likelihood of developing

42:21

Alzheimer's? Well we think we're

42:23

about to publish our first genome-wide

42:25

association on early onset and when

42:28

you add those into the mix

42:30

we probably have about a hundred

42:32

genes that we now know are

42:34

associated with Alzheimer's disease. So

42:36

if you took a sample from somebody and you

42:38

read those hundred genes, how

42:41

accurate could you be with a test

42:43

for whether or not the person, that

42:45

person, is going to get Alzheimer's now?

42:48

Oh well we're a bit clever than that. What we

42:50

do is we take those hundred genes and we look

42:53

at all the other genes that may

42:55

make a contribution and we create

42:57

it with an algorithm that probably

43:00

has thousands of genes involved

43:03

and from that we can predict

43:05

at the extremes with 90% confidence

43:09

whether you will or you won't

43:11

get Alzheimer's disease. However the

43:14

majority of people will be somewhere

43:16

in between in terms of their

43:18

risk. Now that's important because when

43:20

we do find treatments we want to

43:22

identify people at the highest risk that

43:25

we can prevent the

43:27

damage. That's the main, the

43:29

gold name used is to get in

43:31

there before the brain is damaged. So

43:34

I think we can do that now but

43:36

in future the real value of

43:39

that will come when we have

43:41

treatments to help people and use

43:44

that information in a positive way.

43:47

That presumably gives us the if you're

43:49

going to get it or not but can you say

43:51

anything about when yet? That's

43:53

more difficult with a number of

43:56

factors that influence the common form

43:58

of Alzheimer's disease. if you

44:00

have the very, very rare forms of mutations, yes,

44:02

you can. I think it's going to be more

44:05

difficult to do that. But David

44:07

Cameron was recently interviewed when we saw some

44:09

of these new immune modifying drugs were being

44:11

trialled in people without Simon's disease and he

44:13

was saying pretty soon we're going to have

44:15

a test which will tell whether a person

44:17

is going to develop this within the next

44:19

X number of years. Is

44:21

that genetic or does that look mainly at

44:23

the biochemistry of the brain? I

44:26

think that probably would have been a genetic

44:28

test. I mean we've worked with

44:31

a company and there is a test out

44:33

there now. We wanted them

44:35

to use the best information so we

44:37

gave them all our data so that

44:40

we could best predict those at the

44:42

extremes. But the problem

44:44

at the moment is we can't offer

44:46

people much to prevent that development.

44:49

But I think very soon

44:52

we may have more drugs

44:54

or maybe even genetic therapies

44:56

in five or ten years time

44:58

that can influence your risk of

45:01

developing the disease that you can

45:03

take at an early stage. So

45:05

things are moving quickly. The thing that

45:07

strikes me is that while

45:09

all this was going on in your

45:11

life, in the middle of it, you

45:13

suddenly depart and go into politics and

45:16

you become government chief science advisor for

45:18

Wales, second person to do that job.

45:21

Wasn't that the wrong time to

45:23

go into science policy or was

45:25

it? Well I just got

45:27

some funding to do a big collection of

45:29

the early onset dementia so I knew I

45:31

couldn't do a lot of the science for

45:33

about three or four years until we had

45:35

the sample. And

45:38

I wondered why we weren't doing

45:40

so well in Wales with science.

45:42

So I thought yes I'll

45:44

have a go see if I can make

45:46

a difference and I was

45:49

lucky enough to be appointed. And the

45:51

first minister said I want

45:54

you to look at why we

45:56

aren't actually creating as

45:58

many good scientific successes

46:00

and bringing in the funding for

46:02

science as you would expect from

46:04

our population. Go away and have a

46:06

look at that. And that's what

46:08

I did. And what I found is that

46:10

we didn't have enough scientists. It wasn't that

46:13

the scientists were not good. They were actually

46:15

pensioned by their weight, but we didn't have

46:17

enough of them. So what

46:19

I did was get some

46:21

European money and some European structural money,

46:23

and we were able to put about

46:25

50 to 60 million into

46:28

bringing in scientific fellows and

46:30

groups of scientists to come and address

46:33

some of the major issues. A lot

46:35

of them are still there in Wales, I'm

46:37

pleased to say. How did you identify,

46:39

though, that the problem was you just

46:41

didn't have enough scientists? It's easy to

46:43

say that, but how did you attack

46:45

the problem of why Wales is lagging

46:48

a bit and where the actual

46:50

problem lay? Well, we counted the number

46:52

of scientists that were working

46:55

in the various areas, mainly in universities.

46:57

We don't have a lot of centers

47:00

or institutes in Wales. And

47:03

it was obvious that we were low

47:05

mainly in the more expensive areas, actually,

47:08

of medical

47:10

science, computing, engineering,

47:12

and that was the issue. So that's

47:15

what brings a lot of the

47:17

funding into areas from those

47:20

research councils. And that was

47:22

the problem. So the way to solve it is

47:24

to bring in some good

47:26

scientists that could build

47:28

on the strengths that we had, but produce

47:30

the numbers. Effectively be

47:32

a nucleus, then, a nidus around

47:35

which once you've got momentum, there's

47:37

embodied momentum there, and money

47:39

begets money. Exactly. And

47:42

strength begets strength. It's built around the strengths

47:44

that we had. And

47:46

we attracted some really fantastic fellows

47:49

who wanted to come and work with

47:52

individuals already in Wales. And also

47:54

we brought in whole groups

47:56

of individuals working in certain

47:59

areas. But is is

48:01

working but so I must say I

48:03

would hope that that would continue on

48:06

But we need a bit more money

48:08

put into to well science through Welsh

48:10

government actually You did that

48:12

for four years had you had enough

48:14

by then or did you think right? I've I've done what

48:17

I wanted to do because there's a good friend once said

48:19

to me You're best in the job

48:21

in the first couple of years because after that

48:23

the problems become your friends But what she was

48:25

getting at is that you come in with a

48:28

completely blank sheet? No biased opinions. This

48:30

is what I think I want to do Is that

48:32

what happened to you or did you think no I

48:34

need to get back to the Alzheimer's? Well,

48:37

I think it was all the latter

48:39

because at that time the Medical Research

48:41

Council and research Charities

48:43

got together and decided to put a

48:46

lot more money into dementia

48:48

research and I applied

48:50

to Host one of

48:52

these centers and was lucky enough to

48:54

get it and that's why I

48:57

went back So you need to invest in

48:59

research to get the results and and

49:01

this was a great opportunity And

49:03

your present role as the director of

49:05

your institution Where does that put you

49:07

does that put you at the lab bench? Or

49:10

does that mainly put you in your strategic

49:12

role where you can fall back on perhaps

49:14

some of that politics and policy Experience you

49:16

had to then guide I think

49:19

more the latter. I think they would ban me from the lab

49:23

No, I that's that's my

49:25

role is is to to

49:27

look at science In

49:29

an overarching way so to bring

49:32

people together to work more Productively

49:34

to bring more funding in

49:37

but also to try and influence those that

49:39

that can make those decisions and that's probably

49:41

what I'll do a little bit more of

49:44

in the next few years Alzheimer's

49:46

is a terrifying prospect though in terms

49:49

of the risk to the world population

49:51

We're an aging population more people are

49:53

making it to the sort of age

49:55

where they may get Alzheimer's So

49:57

far we've dwelled really heavily on the

50:00

genetics that underpin this, the mechanisms of the

50:02

disease and therefore the risk factors. We haven't

50:04

talked about what the interventions might look like.

50:06

Is that something that you have your eye

50:08

on? Now we're in a position where we

50:10

can tell people what they're going to get

50:13

wrong with them, but their next

50:15

question is going to be what do I do about it? So

50:17

this is what the Centre in Cardi

50:19

C is focused on. So we work

50:21

on Alzheimer's, Huntington's disease and Parkinson's disease.

50:24

So we are taking the

50:26

genetic information on now to understand

50:28

the disease mechanisms. One

50:31

of those that have mentioned is

50:33

the complement system which is about

50:35

inflammation in the brain and

50:38

that is implicated by a number of

50:40

the genes that we have found and

50:42

we are confident that maybe within the

50:44

next five to seven years if we

50:46

can get these complement drugs

50:48

into the brain we will have

50:50

some therapies there because these are

50:52

already used for other diseases. So

50:55

that's Alzheimer's. What about the other

50:57

diseases? I think it's amazing

50:59

things that Vincent Dion in my group

51:01

is doing with Huntington's using

51:04

genetic therapies. You have a

51:06

biological scissors, this CRISPR

51:09

technology that can be

51:11

put into each cell in the

51:13

brain and reduced down this

51:16

region of the Huntington gene

51:18

that if you have repeats

51:21

in this gene, if you have over

51:23

30 repeats you get Huntington's

51:25

disease. If you have less you

51:27

don't and what Vincent

51:30

is doing is cutting that

51:32

area down so

51:34

that it becomes less than 30

51:37

and it's working. It's working in cells,

51:39

it's working in animal models and

51:42

if that works then

51:44

that would cure Huntington's disease in

51:46

a one-off treatment. So

51:49

there's amazing things going

51:51

on and I think genetic therapies in

51:53

a different form can also be used

51:55

for these more common diseases and that's

51:57

something that we're working on also. So

52:00

your hopes for the next five years? I

52:03

think we'll have a much greater understanding of

52:05

the true complexity of this common disease and

52:07

we will have some therapies

52:09

that are, if not in the

52:11

clinic, close to the clinic. And

52:14

how about a reflection on politics,

52:16

policy, that kind of thing? Having dabbled

52:19

in that space, any

52:21

particular things you think in retrospect, I wish I'd

52:23

done that or I'm going

52:25

to lobby for my successor to

52:27

do X? I

52:30

think it's a difficult thing.

52:33

Getting science into politics, we need more of

52:35

it. We also need

52:37

to appreciate that many of

52:39

the ministers and politicians that work

52:42

in this area don't understand science

52:44

and we need to make

52:46

them feel comfortable about asking the

52:48

stupid question because that's important. So

52:51

we need to support as well as advise,

52:53

I think in the short term, until we

52:55

can get more science understanding

52:58

into government. Science

53:01

covers every bit of progress, preferably,

53:03

that's going to come in the next 20 or

53:06

30 years. We really need to get to

53:08

grips with it. Wales is

53:10

former chief scientist and Alzheimer's guru,

53:12

Julie Williams. And that's it

53:15

for this week, The Five Life Sciences

53:17

back at the same time next Sunday

53:19

when we're all aboard for a show

53:21

all about the science of sustainable shipping.

53:23

If you'd like to get in touch

53:26

in the meantime, our email address fivelivescienceatbbc.co.uk.

53:28

Until then from me, Chris Smith. Thank

53:30

you for listening and goodbye. This

53:34

is the story of a powerful Nigerian

53:37

televangelist. He was a huge celebrity and

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he had a way of presenting himself

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as man of God. Who attracted followers

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It was like going to heaven and being

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asked to stay. But once there, some say

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