Ageing

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0:00:03 > 0:00:06Welcome to Bang, unravelling the science behind the issues

0:00:06 > 0:00:08that impact all our lives.

0:00:08 > 0:00:11This week we're tackling ageing.

0:00:11 > 0:00:13People are living longer.

0:00:13 > 0:00:15Back in the '40s, life expectancy in this country

0:00:15 > 0:00:18was set at around 67 years of age.

0:00:18 > 0:00:19Now it's 80 years of age.

0:00:21 > 0:00:24And the consequences of that are rarely out of the news,

0:00:24 > 0:00:28with stories about employment, the cost of pensions and health care.

0:00:30 > 0:00:33Living longer also means that more people will

0:00:33 > 0:00:34suffer from age-related conditions

0:00:34 > 0:00:37like dementia and osteoporosis.

0:00:37 > 0:00:38So the big question is

0:00:38 > 0:00:41if we're living longer, can we live more healthily too?

0:00:43 > 0:00:45Tonight on Bang, the science of ageing.

0:00:48 > 0:00:50Sir Terry Wogan joins the team to sort

0:00:50 > 0:00:53fact from fiction in the news headlines.

0:00:53 > 0:00:56Vitamin E slows down Alzheimer's.

0:00:56 > 0:00:59Vitamin B is a sovereign remedy.

0:00:59 > 0:01:03According to this headline, "Statins halt Alzheimer's."

0:01:03 > 0:01:06There's so much information.

0:01:06 > 0:01:09Three generations of the Hall family take a microscopic

0:01:09 > 0:01:12look at how our muscles and bones change as we get older.

0:01:15 > 0:01:17As I look at Molly, I'm thinking,

0:01:17 > 0:01:19"Well, what's she doing right that I'm not doing?"

0:01:19 > 0:01:21Or maybe it's too late.

0:01:22 > 0:01:26And Liz meets a scientist on the verge of a major discovery.

0:01:26 > 0:01:29Using live human nerve cells is completely

0:01:29 > 0:01:32transforming our understanding of how to find a cure.

0:01:32 > 0:01:36This is the scientific process at its best.

0:01:38 > 0:01:40MUSIC: "My Generation" by The Zimmers

0:01:42 > 0:01:45# People try to put us down

0:01:45 > 0:01:47# Talking about my generation

0:01:47 > 0:01:49# Just because we get around. #

0:01:51 > 0:01:53People are now living longer than ever...

0:01:55 > 0:01:58..and we spend millions trying to cover the cracks

0:01:58 > 0:02:00of our ageing exteriors

0:02:00 > 0:02:03but we all know it's what's on the inside that really counts.

0:02:07 > 0:02:10As we age, our muscles, our bones and our brains

0:02:10 > 0:02:12become more and more vulnerable.

0:02:14 > 0:02:16So, taking a look inside the body,

0:02:16 > 0:02:20we're joined by three generations of the Hall family.

0:02:20 > 0:02:2119-year-old Molly,

0:02:21 > 0:02:23her 52-year-old mum, Judith,

0:02:23 > 0:02:27and granny Mary, who's 88.

0:02:27 > 0:02:28So, what we're going to do

0:02:28 > 0:02:32is to take a look at the ageing process on the cellular level

0:02:32 > 0:02:36and we're going to show you, with people of equivalent ages,

0:02:36 > 0:02:41what is happening right inside your muscles.

0:02:41 > 0:02:45We all know we lose muscle mass and strength as we age

0:02:45 > 0:02:48but what actually is this deterioration?

0:02:48 > 0:02:52This is a muscle section from a young person like Molly

0:02:52 > 0:02:56and what you can see is that there are individual muscle fibres here.

0:02:56 > 0:02:58The most important thing

0:02:58 > 0:03:01is you see that pretty well each fibre looks the same.

0:03:03 > 0:03:06Hidden inside are the mitochondria -

0:03:06 > 0:03:11the power plant within every cell that converts our food into energy.

0:03:13 > 0:03:16Doug has stained the cells to highlight mitochondrial damage.

0:03:16 > 0:03:21A cell with healthy mitochondria will show no bright colours.

0:03:22 > 0:03:26Now, what happens when we go to Judith's muscle biopsy...

0:03:26 > 0:03:32I'm quite shocked, actually, how the differential between Molly and me.

0:03:32 > 0:03:34I'll get you a chair!

0:03:34 > 0:03:38..we'll see that there are changes that have already started to happen.

0:03:38 > 0:03:41You can see that everything isn't the same colour.

0:03:42 > 0:03:47Different colours indicate different types of damage in the mitochondria.

0:03:47 > 0:03:50Doug believes that could be an important

0:03:50 > 0:03:53factor behind shrinkage and cell death and that's what

0:03:53 > 0:03:57leads to the loss of muscle mass we see as we get older.

0:03:57 > 0:04:01So how well has the mitochondria survived in someone of Mary's age?

0:04:02 > 0:04:07This has got even more marked changes, which is associated with

0:04:07 > 0:04:08mitochondrial damage.

0:04:10 > 0:04:13It now looks like Christmas lights, doesn't it?

0:04:15 > 0:04:19Someone of Mary's age could have lost over 50% of their peak

0:04:19 > 0:04:23muscle mass, leading to impaired mobility and poorer quality of life.

0:04:25 > 0:04:27It's important to understand

0:04:27 > 0:04:29the process is going to happen to everybody.

0:04:29 > 0:04:31We're all going to age.

0:04:31 > 0:04:36Is there anything we can do to sort of mitigate this process?

0:04:36 > 0:04:40Well, one of the things we know is that if people do regular

0:04:40 > 0:04:44exercise you can actually move your muscle back to something

0:04:44 > 0:04:46many years before.

0:04:46 > 0:04:49So you could almost suggest that you could almost go back

0:04:49 > 0:04:53to there or, in Judith's case, might even be able to go back to that.

0:04:55 > 0:04:59While some muscle wastage is an inevitable part of ageing,

0:04:59 > 0:05:01a lot of it comes down to the fact that we tend to be

0:05:01 > 0:05:04less active as we get older.

0:05:04 > 0:05:08But regular exercise can build up muscle up to five times faster

0:05:08 > 0:05:09than it wastes away.

0:05:11 > 0:05:16- I like the fact that you can still do something.- Absolutely.

0:05:16 > 0:05:18It's not too late to make a difference.

0:05:20 > 0:05:24But it's not just our muscles that get weaker with age.

0:05:24 > 0:05:27One in five men and one in two women over the age of 50

0:05:27 > 0:05:29will break a bone.

0:05:29 > 0:05:33Hips and arms make up over half of the bones broken in over-60s

0:05:33 > 0:05:38and the consequences can be very serious indeed.

0:05:38 > 0:05:43Every month, 1,100 people die as a result of hip fractures, so

0:05:43 > 0:05:47bone health and osteoporosis are a big concern for the elderly.

0:05:49 > 0:05:52So let's see what happens to our bones as we age.

0:05:53 > 0:05:56Each member of our family have been put in a DEXA scanner.

0:05:59 > 0:06:02This machine beams low doses of X-ray at the patient's body

0:06:02 > 0:06:06giving us accurate measurements of their bone density.

0:06:10 > 0:06:13Right, Molly, it's time to get the results of your DEXA scan

0:06:13 > 0:06:15so shall we just bring them up on the screen?

0:06:15 > 0:06:18Looks a bit odd, doesn't it? Inside of you.

0:06:18 > 0:06:20This is Molly's.

0:06:20 > 0:06:25Someone Molly's age should be somewhere in the light blue area.

0:06:25 > 0:06:27And we can see that you're up there.

0:06:27 > 0:06:32So your bone density is well above the average we'd expect.

0:06:32 > 0:06:34That's good. I'm happy about that.

0:06:34 > 0:06:37Judith has a lower bone density than her daughter,

0:06:37 > 0:06:39which we'd expect because

0:06:39 > 0:06:40you're older.

0:06:42 > 0:06:44As I look at Molly, I'm thinking,

0:06:44 > 0:06:47"Well, what's she doing right that I'm not doing?"

0:06:47 > 0:06:48Or maybe it's too late.

0:06:48 > 0:06:53From the moment we're born, bone density slowly increases,

0:06:53 > 0:06:56reaching a peak at about 30,

0:06:56 > 0:06:59when it levels out then starts to decline slowly.

0:06:59 > 0:07:03At around 50 years old, it dips sharply, but only for women.

0:07:03 > 0:07:06The changes for men aren't as dramatic

0:07:06 > 0:07:08because they don't have the menopause.

0:07:10 > 0:07:14If we go to the other age of 80-something...

0:07:16 > 0:07:19Mary has lost around a third of the bone density

0:07:19 > 0:07:22she would have had at peak bone health.

0:07:22 > 0:07:26As we age, strong bone can become a thin lattice

0:07:26 > 0:07:29and this is one of the reasons that older people are

0:07:29 > 0:07:31so susceptible to breaking bones.

0:07:33 > 0:07:35But there's good news for Mary.

0:07:38 > 0:07:42If we look at the spine, actually, your bone density is a lot higher,

0:07:42 > 0:07:46well above expected for age, at the spine.

0:07:46 > 0:07:47I'm top dog.

0:07:49 > 0:07:53Mary has led an active life, including working on a farm,

0:07:53 > 0:07:56and it looks as if that has paid off.

0:07:58 > 0:08:02- So, you've come out of this very well.- Yes.

0:08:02 > 0:08:06I'm going to make sure I follow in Granny's footsteps.

0:08:06 > 0:08:07Not Mum's.

0:08:07 > 0:08:08THEY LAUGH

0:08:11 > 0:08:16So what causes this decline in bone density as we age?

0:08:16 > 0:08:20First, we need to understand what bone actually is.

0:08:22 > 0:08:26This obviously is a bone. It's the long thigh bone that

0:08:26 > 0:08:30runs from hip joint to your knee and it's called the femur.

0:08:30 > 0:08:34And it looks pretty much like it's made up of one material - bone.

0:08:34 > 0:08:37But it's actually far more complex than that.

0:08:38 > 0:08:42There are several types of bone tissue but the structural

0:08:42 > 0:08:46part of bone is essentially made up of two very different materials.

0:08:46 > 0:08:49The first is collagen, a protein that's found in many

0:08:49 > 0:08:53different forms in our skin and in various tissues in the body.

0:08:53 > 0:08:57And it's an incredibly tough and elastic substance.

0:08:57 > 0:09:00In our bones, it provides flexibility so, just like these suspension

0:09:00 > 0:09:03systems in these old cars, it allows our bones to withstand

0:09:03 > 0:09:07the incredibly dynamic forces that our bodies experience every day.

0:09:12 > 0:09:16'But as a material to help you stand up, collagen is rather useless,

0:09:16 > 0:09:19'which is why bones need a second, harder, material.'

0:09:23 > 0:09:28It's a mineral called calcium phosphate. Now, it is pretty hard

0:09:28 > 0:09:32but it's also incredibly brittle. A bit like this glass.

0:09:34 > 0:09:38Now, on their own, neither would be any good for a skeleton.

0:09:38 > 0:09:41If my bones were made of all collagen they'd be wobbly

0:09:41 > 0:09:43and unstable. If they were made of all calcium phosphate

0:09:43 > 0:09:45they would shatter pretty easily.

0:09:49 > 0:09:52'But it's when those two very different materials combine

0:09:52 > 0:09:54'that something remarkable happens.

0:09:56 > 0:10:00'This old car windscreen is no more than two layers of glass with

0:10:00 > 0:10:03'a see-through layer of rubber sandwiched in-between.'

0:10:05 > 0:10:09The result is a rigid composite material that won't shatter easily.

0:10:11 > 0:10:13A bit like our bones.

0:10:16 > 0:10:20In fact, healthy human leg bones can withstand compressive

0:10:20 > 0:10:22forces of over a tonne.

0:10:23 > 0:10:27Bones are as alive as any other part of our bodies.

0:10:27 > 0:10:30They're constantly changing, renewing and repairing themselves.

0:10:30 > 0:10:33All through life, bone material is being

0:10:33 > 0:10:37released from our skeleton, with new bone being laid down.

0:10:37 > 0:10:41And the released bone matter is broken down, and its minerals,

0:10:41 > 0:10:45like calcium, are released into the body in a process called resorption.

0:10:47 > 0:10:51In fact, by the time you reach your late 30s, your entire

0:10:51 > 0:10:55skeleton will have been resorbed and reformed five or six times.

0:10:57 > 0:11:00And that's a process that will go on until the day you die.

0:11:02 > 0:11:03From our 30s onwards,

0:11:03 > 0:11:08bone formation no longer keeps up with bone loss, so our bones

0:11:08 > 0:11:11lose density and mass. Just like we saw with the Hall family.

0:11:13 > 0:11:16And, unfortunately, for women past the menopause, this loss

0:11:16 > 0:11:18is three times as fast as it is for men.

0:11:20 > 0:11:23So what causes this huge difference in bone density

0:11:23 > 0:11:25between men and women?

0:11:25 > 0:11:27Well, in part, it's down to the hormone oestrogen.

0:11:27 > 0:11:31Oestrogen is the primary female sex hormone.

0:11:31 > 0:11:34It's present in men as well but it's in much lesser concentrations.

0:11:36 > 0:11:40The cells that break down and resorb our bone are called osteoclasts

0:11:40 > 0:11:45and oestrogen helps to slow down their activity.

0:11:45 > 0:11:49But as we women age, we produce less and less oestrogen, with our levels

0:11:49 > 0:11:53dropping far below those of men by the time we reach our menopause.

0:11:53 > 0:11:56And so the suppressing effects that the oestrogen

0:11:56 > 0:11:59has on the osteoclasts are greatly reduced...

0:12:00 > 0:12:03..meaning that more and more bone is resorbed,

0:12:03 > 0:12:06outstripping the amount of new bone that is formed.

0:12:10 > 0:12:13But, the more you use your bones, especially with high impact

0:12:13 > 0:12:18exercise like running, the more bone growth is stimulated.

0:12:18 > 0:12:19And regular exercise

0:12:19 > 0:12:22can decrease your chance of breaking bones by 50%.

0:12:25 > 0:12:30I've been running since I was late 30s, I think.

0:12:30 > 0:12:34Now I swim three times a week and run twice a week.

0:12:34 > 0:12:37On a Monday and a Tuesday, I go to yoga on the bus

0:12:37 > 0:12:40and then I run back against my watch.

0:12:40 > 0:12:45The average age here is 70. There's 350 years of talent here!

0:12:47 > 0:12:52However, a healthy body is nothing without a healthy mind.

0:12:52 > 0:12:57Today, over 800,000 people in the UK are suffering from some

0:12:57 > 0:13:00form of dementia and the chances of developing it increase

0:13:00 > 0:13:02dramatically with age.

0:13:04 > 0:13:06There are up to 100 different types of dementia,

0:13:06 > 0:13:10which is the collective term for symptoms caused by diseases

0:13:10 > 0:13:14like Alzheimer's, vascular dementia and sometimes Parkinson's.

0:13:14 > 0:13:18In most cases, dementia is a result of the loss of connections

0:13:18 > 0:13:21between brain cells, or brain cell death.

0:13:21 > 0:13:25Memory loss, difficulty in problem solving and changes

0:13:25 > 0:13:29in personality are just some of the most common signs of the illness.

0:13:31 > 0:13:33The priority for scientists

0:13:33 > 0:13:37is to work out exactly what's going on inside the brain.

0:13:38 > 0:13:42So I've come to Newcastle University's Brain Tissue Resource

0:13:42 > 0:13:43to find out.

0:13:46 > 0:13:48Do you know, I've done many things in my time

0:13:48 > 0:13:50but I've never held a brain?

0:13:50 > 0:13:52There's a real softness to this.

0:13:54 > 0:13:56You know, it's very delicate.

0:13:57 > 0:14:00This brain is typical of a healthy 80-year-old.

0:14:01 > 0:14:06I still find it very difficult to believe this is

0:14:06 > 0:14:12responsible for everything I think, everything I decide to do,

0:14:12 > 0:14:16for my memories, for my personality.

0:14:18 > 0:14:22And here is a brain of an 80-year-old with Alzheimer's.

0:14:22 > 0:14:24It's about 10% lighter.

0:14:26 > 0:14:28This feels very different to me.

0:14:28 > 0:14:32There's a sense that somehow the texture of this has been altered.

0:14:32 > 0:14:35I mean, certainly the brain is a lot lighter

0:14:35 > 0:14:39because we know we've lost nerve cells from key parts

0:14:39 > 0:14:43of the brain that will make the whole brain function differently.

0:14:43 > 0:14:45Or at least it would during life.

0:14:46 > 0:14:50As the cells die, whole parts of the brain shrivel up

0:14:50 > 0:14:53and one of the first areas to shrink is

0:14:53 > 0:14:55the hippocampus at the bottom of the brain,

0:14:55 > 0:14:58a critical area for memory.

0:14:58 > 0:15:03We know that by the time somebody first shows their first symptoms of

0:15:03 > 0:15:07memory impairment, short term memory usually, that the

0:15:07 > 0:15:10disease process has been going on for a little

0:15:10 > 0:15:15while before that, perhaps 5-10 years. So, by the time somebody shows

0:15:15 > 0:15:20their first symptoms, the pathology and changes are well established.

0:15:22 > 0:15:26For many people over 60, the fear that they may be developing dementia

0:15:26 > 0:15:30or could do so in the future is a major worry.

0:15:30 > 0:15:32And it's rarely out of the press.

0:15:36 > 0:15:40Well, let me break it to you gently. The news is not so good.

0:15:40 > 0:15:47One in three of us over the age of 65 are going to die with dementia.

0:15:48 > 0:15:52And it's even worse for a man of my advanced years at 75.

0:15:52 > 0:15:55By the time I'm 85, there's a 50-50 chance

0:15:55 > 0:15:59I'm going to develop dementia.

0:15:59 > 0:16:01'Well, that scares me so I want to know

0:16:01 > 0:16:03'if there's any way of preventing it.

0:16:03 > 0:16:07'And one thing that keeps popping up in the papers - diet.'

0:16:08 > 0:16:11Numerous reports have shown that this Mediterranean diet

0:16:11 > 0:16:13is going to do you a power of good.

0:16:13 > 0:16:17Improve your brain function, your general health,

0:16:17 > 0:16:20less chance perhaps of developing Alzheimer's disease.

0:16:20 > 0:16:24But diet isn't the only suggestion hitting the headlines.

0:16:24 > 0:16:27In fact, hardly a week goes by without some headline saying

0:16:27 > 0:16:29that there's a new magic bullet.

0:16:32 > 0:16:35Vitamin E slows down Alzheimer's.

0:16:35 > 0:16:38Vitamin B is a sovereign remedy.

0:16:38 > 0:16:42Here's another one extolling the virtues of coconut oil.

0:16:43 > 0:16:47And then we have the magic statins.

0:16:47 > 0:16:52According to this headline, "Statins halt Alzheimer's."

0:16:52 > 0:16:54There's so much information

0:16:54 > 0:16:56and...I haven't a clue!

0:16:58 > 0:16:59But I want to find out

0:16:59 > 0:17:04and I know a scientist who might just help me unravel all of this.

0:17:04 > 0:17:07So, vitamin E, first of all, can that do any good?

0:17:07 > 0:17:10Well, there was some research published recently which

0:17:10 > 0:17:12suggests it might be able to do some good, however

0:17:12 > 0:17:15very, very high doses were used and, actually, many doctors don't

0:17:15 > 0:17:19recommend that people should be taking vitamin E at such high doses.

0:17:19 > 0:17:23'And Simon also tells me research into vitamin B isn't

0:17:23 > 0:17:25'conclusive yet and

0:17:25 > 0:17:29'the effectiveness of coconut oil seems to be hearsay.'

0:17:29 > 0:17:32I think it would be wonderful and amazing to think that the

0:17:32 > 0:17:37answer to dementia would be found in a small bottle such as these.

0:17:37 > 0:17:39Something safe, something cheap.

0:17:39 > 0:17:42Unfortunately, I think, the evidence at the moment doesn't back

0:17:42 > 0:17:47any of this up, certainly enough for people to start taking these.

0:17:47 > 0:17:48'But what about statins,

0:17:48 > 0:17:52'the so-called wonder drug for the over-50s?

0:17:52 > 0:17:55'Statins can help lower cholesterol

0:17:55 > 0:17:58'but what is behind the bold headline that they are also

0:17:58 > 0:18:01'effective against Alzheimer's?'

0:18:01 > 0:18:03Now, this was about a study in mice.

0:18:03 > 0:18:06Not really worried about Alzheimer's in mice.

0:18:06 > 0:18:09Well, that's right. Mice don't get Alzheimer's disease and the mice

0:18:09 > 0:18:12in these experiments didn't have the Alzheimer's disease

0:18:12 > 0:18:15- that we would know. - Is that any good to us, then?

0:18:15 > 0:18:18It suggests that there could be a possible mechanism.

0:18:18 > 0:18:20What certainly isn't true is that

0:18:20 > 0:18:23statins halt Alzheimer's disease or other dementias.

0:18:24 > 0:18:27'So have there been any trials in humans?'

0:18:27 > 0:18:29There have been some reports recently but I don't think

0:18:29 > 0:18:32it's conclusive yet and I think we'll have to wait a little

0:18:32 > 0:18:34longer until we have more evidence before we can say for certain.

0:18:34 > 0:18:36Is there any prospect that we're going to get

0:18:36 > 0:18:40a treatment that will work for Alzheimer's?

0:18:40 > 0:18:43I think there is certainly a good deal of optimism that we will

0:18:43 > 0:18:47manage a treatment that does something to Alzheimer's by 2025,

0:18:47 > 0:18:49and it may even be before then.

0:18:49 > 0:18:50Well, thank heaven for that!

0:18:50 > 0:18:53A little light at the end of the tunnel.

0:18:55 > 0:18:57'In the meantime, we'll just have to wait.'

0:18:59 > 0:19:03So, I'm afraid no easy solution.

0:19:04 > 0:19:07And, although I normally stick to an Irish diet, I think

0:19:07 > 0:19:11in future I'd better take the advice of better men,

0:19:11 > 0:19:17and go for the olive oil, the vegetables, the fruit.

0:19:17 > 0:19:19How hard can it be?

0:19:21 > 0:19:24We've been told for some time that exercise

0:19:24 > 0:19:26and diet help to prevent disease

0:19:26 > 0:19:29and there's a lot of research to back this up.

0:19:29 > 0:19:31Here's just one example.

0:19:31 > 0:19:34In a particular study that lasted 30 years

0:19:34 > 0:19:37and monitored the health of almost 2,500 men in Caerphilly

0:19:37 > 0:19:40in Wales, the results were very interesting.

0:19:40 > 0:19:44The data suggest that those that led a much healthy lifestyle were

0:19:44 > 0:19:49substantially less likely to develop strokes, heart disease or diabetes.

0:19:49 > 0:19:53And the risk of developing dementia was reduced by about 60%

0:19:53 > 0:19:56and, for those men that did go on to develop dementia,

0:19:56 > 0:19:59the onset was delayed by up to seven years.

0:20:02 > 0:20:04Although ageing at the moment might be

0:20:04 > 0:20:08perceived by many as an inevitable downhill process, you can

0:20:08 > 0:20:11still have some control about how steep the hill is.

0:20:13 > 0:20:17Nevertheless, caring for and treating those with dementia is

0:20:17 > 0:20:21currently costing the UK over £23 billion a year.

0:20:21 > 0:20:25That's more than heart disease, cancer or strokes.

0:20:25 > 0:20:33And figures are expected to rise to 1.7 million people by 2050,

0:20:33 > 0:20:37which is why David Cameron recently pledged at the G8 summit to

0:20:37 > 0:20:39increase the amount spent on research.

0:20:41 > 0:20:44The aim of trying to find a cure or disease-halting

0:20:44 > 0:20:48therapy by 2025 is within our grasp.

0:20:50 > 0:20:52And it may be closer than we think.

0:20:53 > 0:20:57'At the Gurdon Institute in Cambridge there is some astonishing

0:20:57 > 0:21:00'research that I can't wait to see for myself.'

0:21:01 > 0:21:03Up to now, the only way to

0:21:03 > 0:21:06study the disease has been either look at brains from people

0:21:06 > 0:21:09who had died of the disease, which is useful, but you're not

0:21:09 > 0:21:13seeing the disease, you're seeing the end point. So we needed a way

0:21:13 > 0:21:16to look in human nerve cells in real-time as the disease progresses.

0:21:18 > 0:21:21So they did something amazing.

0:21:21 > 0:21:24Building on pioneering research done here 50 years ago,

0:21:24 > 0:21:27they took stem cells, the sort of cell that can form any other

0:21:27 > 0:21:31type of cell, and made them develop into brain cells.

0:21:34 > 0:21:37They're all talking to one another and they talk the same way they do

0:21:37 > 0:21:39in your brain or my brain. These are live.

0:21:39 > 0:21:42I know you do this every day, right. It's kind of... You're used to

0:21:42 > 0:21:45this but it's mind-blowing what's going on in this laboratory.

0:21:45 > 0:21:47The fact that you can do this is humongous, isn't it?

0:21:47 > 0:21:50Yes, it's great fun. I mean, this is two-dimensional.

0:21:50 > 0:21:52- Great fun!- No, it is. But also, the other thing

0:21:52 > 0:21:53we're working on is, you know, the brain

0:21:53 > 0:21:57is three-dimensional, so we're also busy trying to make this in three

0:21:57 > 0:22:00dimensions as well, just get all the architecture, so making mini brains.

0:22:00 > 0:22:03I mean that's a little bit crazy. Are you telling me that,

0:22:03 > 0:22:05- in a Petri dish, you can actually have a 3D brain?- Yeah.

0:22:07 > 0:22:10'Rick uses stem cells from someone who is genetically almost

0:22:10 > 0:22:12'certain to get Alzheimer's

0:22:12 > 0:22:16'and he can effectively grow the disease in his lab.'

0:22:16 > 0:22:18If you look at the brain of someone with Alzheimer's disease

0:22:18 > 0:22:21and cut a little slice, you can find two bits of pathology

0:22:21 > 0:22:24and they are called plaques and tangles.

0:22:24 > 0:22:28'For the first time, Rick can now watch them as they form.

0:22:28 > 0:22:32'Plaques are made up of tiny fragments of protein,

0:22:32 > 0:22:35'which stop the nerve cells communicating with each other,

0:22:35 > 0:22:37'causing the symptoms of dementia.'

0:22:38 > 0:22:43This is plaque formation that is characteristic of Alzheimer's.

0:22:43 > 0:22:46Exactly. So this is completely abnormal.

0:22:46 > 0:22:47So these are very sick neurones.

0:22:48 > 0:22:52'Tangles are involved in the spread of the disease.

0:22:52 > 0:22:54'They are made up of a different protein,

0:22:54 > 0:22:56'present inside the brain cells.'

0:22:58 > 0:23:01In the disease, it actually just starts accumulating and forming

0:23:01 > 0:23:05these big, long tangles which essentially strangle the neuron.

0:23:05 > 0:23:07But the other thing it does is we all now think it

0:23:07 > 0:23:11spreads from neuron to neuron, making the other neurons sick.

0:23:11 > 0:23:13'In another lab, Rick can

0:23:13 > 0:23:17'watch the tangle protein passing on the disease.'

0:23:17 > 0:23:20It's not like an infection, where a virus or a bacterium...

0:23:20 > 0:23:22This is a protein - the simplest thing you could possibly use.

0:23:22 > 0:23:25This is your body turning on itself.

0:23:25 > 0:23:28Why is it important to understand this?

0:23:28 > 0:23:30We think this is a fundamental mechanism how the disease

0:23:30 > 0:23:32spreads through your brain.

0:23:32 > 0:23:36And it's only because they can grow living brain cells that

0:23:36 > 0:23:39they've been able to see the disease spreading.

0:23:41 > 0:23:45This means Rick and his team can, for the first time, test a whole

0:23:45 > 0:23:49multitude of different drugs on live human brain cells

0:23:49 > 0:23:51and watch the effects on a cellular level.

0:23:53 > 0:23:56At the moment, over 1,000 drugs are being investigated.

0:24:00 > 0:24:03How long before you are able to say to the pharmaceutical industry,

0:24:03 > 0:24:06"This is one that is looking exciting - start making it?"

0:24:06 > 0:24:09We're very close. We're now in the process of working out

0:24:09 > 0:24:10which one or two to really put our money on.

0:24:10 > 0:24:12That's within this year, effectively.

0:24:12 > 0:24:14- Within this year?- Yeah. - That's exciting stuff.

0:24:16 > 0:24:20A life-changing treatment for Alzheimer's is now closer than ever.

0:24:20 > 0:24:24You know this is a scientific process at its best.

0:24:24 > 0:24:28Ground-breaking research that was carried out 50 years ago has

0:24:28 > 0:24:30now inspired others to apply that knowledge to find

0:24:30 > 0:24:34a cure for a debilitating disease and it's a very exciting

0:24:34 > 0:24:38time for Alzheimer's research because this breakthrough, allowing

0:24:38 > 0:24:43us to understand the disease at its early stages using live human nerve

0:24:43 > 0:24:47cells, is completely transforming our understanding of how to find a cure.

0:24:49 > 0:24:52The goal is to be able to live healthier lives

0:24:52 > 0:24:56without diseases like osteoporosis and dementia.

0:24:56 > 0:24:58But how long could we live?

0:24:58 > 0:25:00How much longer would we want to live?

0:25:02 > 0:25:05There is some very intriguing research that's exploring

0:25:05 > 0:25:08what it actually is that limits our life span.

0:25:10 > 0:25:11Instead of trying to understand

0:25:11 > 0:25:13human ageing, if you could just

0:25:13 > 0:25:15take a really simple animal,

0:25:15 > 0:25:18the simplest animal possible that shows ageing,

0:25:18 > 0:25:21and then figure out what ageing is in that

0:25:21 > 0:25:24organism, that at least would give you a start.

0:25:27 > 0:25:30Professor Gems has been studying worms.

0:25:30 > 0:25:34He's working with the microscopic C elegans roundworm.

0:25:34 > 0:25:36Each Petrie dish contains thousands.

0:25:38 > 0:25:41C elegans were the first multi-cellular organisms to

0:25:41 > 0:25:44have their entire genome sequenced.

0:25:44 > 0:25:47They only consist of 1,000 cells

0:25:47 > 0:25:53but, amazingly, they still share 40% of the same genes as us.

0:25:53 > 0:25:55Their life spans are really short.

0:25:55 > 0:25:59They actually only live 2-3 weeks so they actually grow old and die

0:25:59 > 0:26:02within 2-3 weeks, which, for a scientist, is absolutely great.

0:26:02 > 0:26:04So you can find answers very quickly?

0:26:04 > 0:26:07Well, that's the point.

0:26:07 > 0:26:09An astonishing discovery showed that

0:26:09 > 0:26:13C elegans with certain genetic mutations were living longer.

0:26:14 > 0:26:18So what you can do is you can isolate worms where one of the genes

0:26:18 > 0:26:21is busted and the worms live longer.

0:26:21 > 0:26:26How long has your most long-lived worm lived?

0:26:26 > 0:26:30Well, my longest-lived worm... I was very proud of it at the time.

0:26:30 > 0:26:35It was a male one that lived about seven times longer than normal.

0:26:35 > 0:26:38So normally it would be living about 2-3 weeks

0:26:38 > 0:26:41and it was seven-fold greater than that.

0:26:41 > 0:26:45So, if it was a human being, it would be living to 800-900 years.

0:26:46 > 0:26:50Intensive investigations came up with a revelation.

0:26:52 > 0:26:56The genes that control ageing in the worm, it turns out that those

0:26:56 > 0:27:01same genes actually exist in humans and, in fact, there is

0:27:01 > 0:27:03now evidence that at least some of the genes that control ageing

0:27:03 > 0:27:06in the worm may even be controlling human ageing,

0:27:06 > 0:27:09- which is very exciting. - It's extremely exciting.

0:27:09 > 0:27:12The implications for us could potentially be enormous.

0:27:14 > 0:27:15I've got to ask you, you know,

0:27:15 > 0:27:19how long before, "We've found it, the answer to ageing?"

0:27:20 > 0:27:24Boy, that's a hard one. The thing which remains unsolved is

0:27:24 > 0:27:28really how those genes are actually producing the increase in life span.

0:27:28 > 0:27:30That's the great big unknown,

0:27:30 > 0:27:32which is what actually is ageing as a process?

0:27:32 > 0:27:37What exactly is it that we die of? That's really an unsolved question.

0:27:44 > 0:27:47The science of ageing is a surprisingly recent

0:27:47 > 0:27:49area of research and it's only

0:27:49 > 0:27:53since the '80s that people have been thinking about it as a disease.

0:27:53 > 0:27:54By taking that approach

0:27:54 > 0:27:57and by studying simple organisms like C elegans,

0:27:57 > 0:28:01Professor Gems is contributing a great deal to our understanding

0:28:01 > 0:28:04of what the principles of ageing really are.

0:28:04 > 0:28:05And once we know that,

0:28:05 > 0:28:07things are going to get very interesting in this field.

0:28:09 > 0:28:11Next time on Bang Goes The Theory,

0:28:11 > 0:28:14flu - is it a case of winter sniffles

0:28:14 > 0:28:17or a full-blown killer virus?

0:28:17 > 0:28:20And, meanwhile, if you fancy working in ageing research,

0:28:20 > 0:28:24check out our careers guide at bbc.co.uk/bang.

0:28:24 > 0:28:27And to take part in an open debate of ageing and ageism,

0:28:27 > 0:28:30follow the links through to the Open University website

0:28:30 > 0:28:32and join the discussion.