Curing Alzheimer's Horizon


Curing Alzheimer's

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Our memories make us who we are,

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but it's thought 30 million people today are losing them

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due to the curse of our time - Alzheimer's.

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Despite their best efforts, scientists have, until now,

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failed to stop this disease,

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but the latest generation of research has unleashed a new front

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in the war against this devastating disease.

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This is a very exciting time.

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There's a new window of opportunity.

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New technology allows us to see

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the signs of Alzheimer's disease earlier than we ever could before.

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Today, a series of drugs trials have been launched across the world,

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drugs that are targeting the disease in its early stage.

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We believe that this trial marks the dawn of a new era

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in Alzheimer's prevention research.

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Initial results are exciting.

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They reveal that there are drugs which are reducing

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signs of the disease.

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Scientists are confident that a cure is tantalisingly close.

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If we treat early enough, we may stave off Alzheimer's disease

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completely and we may never have to worry about it again.

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Horizon asks - can we end the curse of Alzheimer's forever?

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"I won't need a shopping list this week. I'll just...

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"I'll remember that." And then you get halfway round a supermarket

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and you think, "What did I have on that list?

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"What did I have to get? I know there's something."

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"Why have I gone upstairs?

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"Have I come up for something, have I left it behind?

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"Was it not upstairs in the first place?"

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I remember faces and I'm still good at that, but not names.

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As we grow old, we all start to forget things,

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but in the back of our minds, there hangs a terrible fear.

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My mother has Alzheimer's,

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so if you've had a day of forgetting a few things, you do get

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gripped with a sort of panic that this is it, this is the beginning.

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About every four minutes, somebody new is told they have the disease.

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The panic grows as the epidemic sweeps across the globe.

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Alzheimer's disease is now one of the most feared medical

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conditions, particularly in people over the age of 45.

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And that's understandable, because we now, tragically,

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most of us know somebody

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who has got Alzheimer's disease.

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This degenerative brain disease leads to a loss of memory

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and eventually the loss of most other brain functions.

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Horizon meets five ordinary people

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whose lives are overshadowed by Alzheimer's.

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Each one in their own way is making an extraordinary

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contribution in the worldwide war against the disease.

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Can you tell me what letter that is?

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In London, Tom has a rare form of Alzheimer's

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which baffled his doctors.

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My brain doesn't compute what they are.

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It's a sort of a jumble.

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It's not, it doesn't mean anything.

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New scanning technology is revealing what's happening in his brain.

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In Phoenix, Arizona, Jamie lives in fear.

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My great-grandmother had Alzheimer's disease.

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Her daughter had Alzheimer's

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and then my two great-uncles also died of Alzheimer's.

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And then my father just recently died a couple of years ago

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with Alzheimer's.

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The gene she carries dramatically increases her

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risk of developing Alzheimer's.

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It's the target of a new generation of research.

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Oh, they're ruined. They're absolutely burnt to a cinder.

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In North Wales, the disease means Gareth is retraining his brain

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so that he can continue to live independently.

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IN SPANISH:

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In Columbia, Flor's family carries a rare genetic mutation

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which causes Alzheimer's at a very early age.

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Her sister already has it.

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New research could prevent Flor from ever developing the disease.

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And in New England, Neil believes a breakthrough drug

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has transformed his life.

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I mean, I don't know what else to attribute it to,

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you know, unless there's a miracle I'm unaware of.

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All these people face a threat of Alzheimer's.

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The disease has long been hard to study, but scientists have recently

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made great advances in understanding how it affects the brain.

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Inside a healthy brain, there are billions of cells called neurons.

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Our thoughts and emotions are transmitted between them

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via connecting synapses.

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But in an Alzheimer's brain,

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a protein starts to build up in the synapses,

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blocking the electrical signals and disrupting the flow of information.

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This protein is called amyloid beta.

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As the disease progresses, it continues to accumulate

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and creates huge sticky clumps called plaque.

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Even at this stage, there can be no apparent symptoms.

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For some reason, the brain can tolerate a certain

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level of amyloid for a number of years, possibly many years.

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And it's as though the amyloid, which may be driving the process,

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needs something else to then go on to produce that

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destruction of brain cells that causes the symptoms

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and the devastation at the individual level.

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The culprit is thought to be another protein inside the brain cell.

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It's called tau.

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Tau normally functions in brain cells like the railroad track

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to take critical nutrients

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up and down brain cells.

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As these tracks disintegrate,

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the supply of nutrients to the neuron is stopped.

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The tau then forms into tangles

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which kills the cell.

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It may take 15 years from the onset of the disease

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for the tau to start creating tangles

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and only then do the symptoms of the disease start to appear.

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The new era of research is focusing on treating

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the disease in its earlier stages.

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This work is happening in some surprising places.

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Medellin, a city dominated by the Andes mountains of Colombia

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in South America.

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It's been notorious for clandestine drug smuggling and kidnappings,

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but its people hold a darker, older secret.

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At its heart are a group of families

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and they may hold the key to the future of Alzheimer's research.

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IN SPANISH:

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Flor lives with her daughter Danielle and her sister, Olga.

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Olga is only 47, but in 2013 she was diagnosed with Alzheimer's.

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Olga is not the only one in Flor's family who has developed

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Alzheimer's in their forties.

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This family carries a gene mutation which can be traced back to

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an ancestor who arrived from Spain 400 years ago.

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Carriers of this gene start to develop the first

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symptoms as early as 45.

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It used to be thought they'd been cursed by a wicked witch

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but - in the 21st century - their plight has captured the attention

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of one of the leading researchers in the field, Dr Eric Reiman.

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Meeting almost a thousand family members for the very first

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time was a life-changing experience.

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To see what those families have gone through,

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not only the clinically-affected person

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but the entire family who has rallied around their loved one

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to provide care, and the impact that it has had on their lives.

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It underscored the urgency we should all

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have in the fight against Alzheimer's disease.

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Flor and her family live with the disease every day.

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Flor's sister Olga has to be looked after by her 70-year-old mother.

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The disease forced Olga to give up work two years ago.

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THEY LAUGH

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For centuries, these families in Colombia have suffered helplessly

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from the ravages of the gene mutation,

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but now they are at the forefront of the new era of scientific research.

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We have this wonderful relationship with families in Colombia

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sharing this common interest.

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We all find it a privilege to think about how we can advance

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the fight against Alzheimer's disease in a way that

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actually helps these families along the way.

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In Colombia, Dr Reiman and the Banner Institute are partners

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in a massive new drugs trial,

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the first-ever major Alzheimer's prevention trial in the country.

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He hopes it'll stop any more members of these

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families from developing the disease.

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Unfortunately, it'll be too late to help Olga.

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IN SPANISH:

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Most of the time, Olga is unaware of the severity of her condition,

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but occasionally she realises what is happening to her.

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Her family is determined to protect her from the horrors of the disease.

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They want to wrap her in their love and support.

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SHE SOBS

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The genetic mutation which afflicts the families in Colombia

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offers a rare opportunity for research

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into the earlier stages of the disease.

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But there is another more common gene which is

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also attracting the attention of the Alzheimer's researchers.

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It's called APOE4.

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Carriers have an increased risk of developing the disease

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later in life, in their seventies.

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One of the largest centres for the genetic

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investigation into the disease is in Phoenix, Arizona.

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Scientists here are searching for people who carry

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this more common gene.

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Jamie Tyrone is a 55-year-old retired nurse.

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She has known about the disease most of her life.

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I have a very, very strong family history of Alzheimer's disease.

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My first memory was when I was ten years old and I visited

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my great-grandmother, who was my first exposure to Alzheimer's.

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She was in a wheelchair and had no cognition

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and her eyes were very empty.

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The next person to get Alzheimer's was her daughter,

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my grandmother, and here's a picture of her.

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And then her two brothers, my two great-uncles,

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also died of Alzheimer's.

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And then my father just recently died a couple of years ago

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with Alzheimer's.

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So, you kind of have the whole picture right here with my family.

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Because of her family history,

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six years ago Jamie decided to find out which genes she carried.

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She sent off a sample of her DNA to be tested.

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Dr Eric Reiman's institute is focusing on the APOE4 gene,

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because it's so closely connected to the way the disease progresses.

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APOE4 has a number of effects on the brain, several of which could

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contribute to the development of Alzheimer's disease.

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The leading theory is that it leads to the development of Alzheimer's

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disease by reducing our ability to get rid of amyloid in the brain.

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His colleague, Dr Jessica Langbaum, has calculated the increased

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risk carriers of the APOE4 gene face of developing Alzheimer's.

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If you have two copies of the APOE4 gene, meaning you have one copy from

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Mum and one copy from Dad, your risk of developing Alzheimer's dementia

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in your lifetime is approximately 30 to 55%.

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If you have one copy of the APOE4 gene,

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your risk is approximately 20 to 25%.

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And if you have zero copies,

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your risk is approximately 10% to 15%.

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Not long after Jamie had sent off her DNA results,

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she received a reply.

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One night, I get a message in my e-mail,

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letting me know that my study results had come in.

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And what you can see here is that I have two copies of the APOE4 gene.

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Jamie's discovery that she carried a double copy of the gene,

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which massively increased her chance of getting the disease,

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drove her to despair.

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When I did find out my genetic status, I didn't have any genetic

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counselling at all and it was quite anxiety-provoking.

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I was told not to talk about it

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for fear that I'd be discriminated against.

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I didn't know what to do with this information and I didn't

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want my family to go through what we had previously had gone through.

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And it came to a part of my life

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where I had to decide what road to take.

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Do I take the dark road and...

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..possibly leave this earth?

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Or do I make meaning of it and take the bright road?

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The carriers of the gene do bear a terrible burden,

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but in the new era of research into the early stage of the disease,

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they have a special role to play.

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It's hard for researchers to identify

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participants for trials who may have the disease in its early stages,

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before the symptoms appear.

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But by working with APOE4 carriers, who are most likely to develop it,

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they dramatically increase their chances.

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Now the Banner Alzheimer's Institute has launched a drugs trial

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aimed at APOE4 carriers like Jamie.

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I'm very hopeful and excited about this trial.

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For the first time in history, we are

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now doing clinical trials on people who are at

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high risk for developing the signs and symptoms of Alzheimer's disease.

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Up until this point, people had to wait until they had memory

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and thinking problems or had a diagnosis,

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until they were given access to a clinical trial.

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Now we are giving clinical trials,

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offering clinical trials to people who are at high risk

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to see if we can stave off the onset of the disease.

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MUSIC: Got To Give It Up By Marvin Gaye

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Jamie is still too young to join the trial.

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However, the new research gives her great hope.

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When you look at the APOE status and the increased risk

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and be able to merge the two together, and really create

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studies specifically for us, is very exciting and very promising.

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And I hope in my lifetime that there will be a prevention or cure.

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I do not know, but if there is,

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I'm very touched to be a part of that process.

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-APPLAUSE

-That's hard.

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The trials are accelerating new research into how to slow down

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and even prevent the disease.

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But the new era also aims to understand what is happening

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inside the brains of sufferers

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as the disease develops from its earlier stages.

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Until now, scientists have only been able to work with

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the brains of Alzheimer's patients once they have died.

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In Colombia, families who carry the Alzheimer's gene mutation

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have played their part in advancing knowledge of the disease.

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When Flor's father died of Alzheimer's, aged 52,

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the family donated his brain to be studied.

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IN SPANISH:

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Dr Francisco Lopera has built up a bank of 200 brains

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donated from patients.

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Until recently,

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these brains have been his only way of investigating the disease.

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IN SPANISH:

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For most of the last 100 years,

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doctors could only research the disease by doing brain autopsies.

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This limited their understanding to the later stages of Alzheimer's.

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Now, new scanning technology has changed all that.

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It allows scientists to identify what's happening in the brains

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of sufferers in the earlier stages of the disease.

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Tom Jarvis is helping scientists reveal

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the effectiveness of this new technology.

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The 72-year-old former railway engineer from Derby

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has come to London with his wife, Hazel.

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He has a very rare form of Alzheimer's

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which was misdiagnosed for two years.

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In the very first place,

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I was being treated for having a lazy eye which affected my reading.

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He was prescribed vari-focals

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and they seemed to make things worse.

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And yes, you went to see the ophthalmologist

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and you had an eye operation, didn't you,

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in February 2013?

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And that didn't work. And then he was discharged.

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His doctors were unable to identify that Tom was having problems

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not in his eyes but in his brain.

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But fortunately for him, he was referred to Professor Nick Fox.

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Normally, Alzheimer's disease starts with problems with memory

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and that's the disease affecting the hippocampus early on,

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but it doesn't always have to.

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The disease can start at the back of the brain,

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areas to do with visual processing, and then it is even more

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likely that people have trouble getting a diagnosis.

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Professor Fox has invented a technique comparing

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a sequence of yearly scans which track the progress of the disease.

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He was able to give Tom a correct diagnosis.

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What we see is how tightly packed this is here,

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but you might be able to make out that the back, there's a little

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bit more space that you can see there than you might have expected.

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That's in exactly the areas that you've been experiencing problems.

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And that's the area which is to do with

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processing of visual information, also related to calculation

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and complex hand movements.

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That is last year and this is the change over one year.

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And that's the second scan, first, second.

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What you see is this fluid-filled space here increasing as we go

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from the first to the second and that is because

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there is brain loss here at the back,

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which reflects the progressive nature of this problem.

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The scans are essential in understanding the early

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stages of the disease.

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The new technology has allowed us to see

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a window of maybe a decade before those symptoms.

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And that's where the new trials are starting to target.

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We hope to have trials of promising treatments when people are well

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and when they have the most, in terms of brain cells, to save.

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That's the window of opportunity.

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-Good, have a seat.

-Thank you.

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Professor Fox and his team want to find out how the disease

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affects the functioning of Tom's visual processing.

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First, I'd like to test your vision if that's all right?

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Can you tell me what letter that is?

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The letters have been fragmented to find out

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if Tom can identify a shape from a complex visual image.

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My guess is it's an F.

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Good guess.

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Looks like an F again.

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Looks like an F?

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If I trace it out with my finger, does that help?

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Ah, is it an R? No?

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It's like an R. It's a P.

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Oh, right.

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The tests show that his brain's ability to process images

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is deteriorating.

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My brain doesn't compute what they are.

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It's a sort of a jumble, it's not, it doesn't mean anything, really.

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It's just little black squares joined together.

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Next, I'm going to say three words

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and if you could just repeat them back to me

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and then remember them, because I'll ask you again in a moment, OK?

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Bus, table, rose.

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Bus, table, rose.

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The team investigates

0:25:130:25:15

how other parts of Tom's brain are being affected,

0:25:150:25:17

especially those more commonly associated with Alzheimer's,

0:25:170:25:22

like memory.

0:25:220:25:23

What were the three words that I asked you to say?

0:25:230:25:26

The last one was rose.

0:25:330:25:35

That's right.

0:25:350:25:36

I can't remember.

0:25:400:25:42

The tests show that the disease is spreading.

0:25:430:25:47

Scientists have, until now, been using scans to understand how

0:25:500:25:54

amyloid plaque affects the various stages of the disease,

0:25:540:25:58

but the new techniques allow them to investigate the other culprit - tau.

0:25:580:26:03

So Tom undergoes a lumbar puncture,

0:26:040:26:07

which draws out spinal fluid

0:26:070:26:09

containing tau from the brain.

0:26:090:26:11

The lumbar puncture today will tell us how much tau is elevated and that

0:26:110:26:17

will tell us how much tau is being released from those brain cells.

0:26:170:26:23

I would guess it might be two or three times what the

0:26:240:26:28

normal range might be.

0:26:280:26:30

How does that feel to you at the moment?

0:26:300:26:32

The lumbar puncture shows the levels of tau,

0:26:320:26:35

but Professor Fox's team want to identify exactly where it is

0:26:350:26:39

in the brain.

0:26:390:26:40

They use cutting-edge scanning to do so.

0:26:400:26:43

First, a radioactive liquid containing a marker

0:26:430:26:47

is injected before scanning.

0:26:470:26:49

Three, two, one - go!

0:26:490:26:52

What's being injected is a tracer

0:26:520:26:55

that has a radioactive probe attached to it.

0:26:550:26:59

The tracer will circulate round the body, enter into the brain and

0:26:590:27:04

will attach if there is tau there and therefore it gets stuck there.

0:27:040:27:09

For the first time, images are revealing which

0:27:090:27:12

parts of the brain are affected by the tau tangles.

0:27:120:27:15

So what we see here in these bright colours,

0:27:150:27:19

those are areas where the tracer has stuck to the tau protein.

0:27:190:27:25

And the bright colour is that radioactivity,

0:27:250:27:27

which is how we detect it.

0:27:270:27:29

And what we're seeing here in this area, which is the

0:27:290:27:32

hippocampus which is critical for memory, we see just full of tau.

0:27:320:27:38

And we think that tau is in some ways more closely related

0:27:380:27:44

to the damage that is critical in Alzheimer's disease

0:27:440:27:47

than its partner in crime, amyloid.

0:27:470:27:49

This research technology is bringing astonishing new insights into how

0:27:500:27:55

the disease builds up in the brain, and then destroys its functions.

0:27:550:28:00

But new research is also revealing that there are changes

0:28:030:28:07

we can make in our daily lives which could significantly reduce

0:28:070:28:11

the chances of developing Alzheimer's.

0:28:110:28:14

Professor Matthew Walker from University of California

0:28:190:28:23

is investigating how plenty of deep sleep could

0:28:230:28:26

preserve our memories and help fight off the disease.

0:28:260:28:30

So, what we've known for some time now is that as we get older,

0:28:300:28:33

our learning and memory abilities start to decline,

0:28:330:28:36

but what we've also known is that a physiological signature

0:28:360:28:41

of ageing is that your sleep starts to get worse.

0:28:410:28:44

And so, based on how important sleep is

0:28:440:28:47

for effectively hitting the save button on new memories,

0:28:470:28:50

we wanted to explore whether that sleep deterioration

0:28:500:28:54

in ageing and in Alzheimer's disease is not simply a symptom

0:28:540:28:58

of the process, but perhaps a cause of the underlying memory problems.

0:28:580:29:03

His work is based on research into the brains of mice,

0:29:050:29:08

which shows that during deep sleep, amyloid is cleared from the brain,

0:29:080:29:14

while too little deep sleep may cause it to build up.

0:29:140:29:17

Professor Maiken Nedergaard has made an astonishing new discovery

0:29:200:29:24

which explains why this happens.

0:29:240:29:26

Her scans of mouse brains found small gaps between neurons.

0:29:260:29:30

These expand by up to 60% when the mice are asleep.

0:29:300:29:35

The gaps allow spinal fluid to sweep through the brain,

0:29:350:29:39

clearing out the waste products.

0:29:390:29:41

As soon as the animal fell to sleep, it was turned on,

0:29:410:29:45

almost like a dishwasher, where these gaps open up and suddenly

0:29:450:29:49

you see the fluid fluxes

0:29:490:29:51

that enter the brain and flushing all the toxic waste product

0:29:510:29:56

the brain produce when we are awake out when we sleep.

0:29:560:30:00

The left scan is a mouse brain when awake, but on the right,

0:30:000:30:05

we see the spinal fluid washing through when asleep.

0:30:050:30:08

Professor Nedergaard has named this the glymphatic system.

0:30:080:30:13

Here we see a sleeping rodent brain

0:30:130:30:15

and we can see the glymphatic system working.

0:30:150:30:18

So, you see the fluid flowing into the brain

0:30:180:30:21

and literally washing beta amyloid away.

0:30:210:30:23

The same thing happens in humans.

0:30:290:30:31

During the day, amyloid builds up in our brains

0:30:310:30:34

and if we don't have regular deep sleep, it starts to accumulate.

0:30:340:30:40

And we need eight hours of good sleep to actively clean up

0:30:400:30:43

the amyloid that build up when we are awake.

0:30:430:30:46

It's clear that the amyloids start to aggregate very early in life

0:30:460:30:53

and if we don't have the long, eight-hours continuous sleep

0:30:530:30:57

when we are young, when we are middle aged,

0:30:570:31:00

we risk that amyloid will build up when we're older.

0:31:000:31:03

Sleep seems to play a crucial role

0:31:030:31:05

in preventing the accumulation of amyloid.

0:31:050:31:08

So Professor Walker is

0:31:080:31:10

trying to find ways of artificially inducing deep sleep.

0:31:100:31:14

Success could slow the development of disease

0:31:140:31:17

and strengthen our memories.

0:31:170:31:20

To start with, he's experimenting with younger brains.

0:31:200:31:24

Chris is a research graduate.

0:31:240:31:26

-Good to meet you.

-Good to be here.

0:31:260:31:29

First, he is asked to memorise connections between faces and words.

0:31:290:31:33

OK, Chris.

0:31:330:31:35

So, what we're going to do is a learning and memory test.

0:31:350:31:37

So, what you'll see on the screen in front of you are some faces

0:31:370:31:41

and underneath there will be a word.

0:31:410:31:44

And your job is to try to connect those two things,

0:31:440:31:47

to learn that those two things are associated together.

0:31:470:31:50

And then later, we'll come back and test you.

0:31:500:31:53

Professor Walker also wants to find out whether a newly-developed

0:32:070:32:12

magnetic brain stimulator can enhance sleep and memory.

0:32:120:32:16

First, Chris's brain is mapped

0:32:160:32:19

to make sure the magnetic pulses are correctly targeted.

0:32:190:32:23

Then two magnets are placed over his head.

0:32:230:32:26

So, the machine itself is going to insert pulses

0:32:260:32:30

of magnetism into the brain and stimulate those brain cells

0:32:300:32:33

and the pathways that we know are critical for sleep and memory.

0:32:330:32:37

So, what we're trying to essentially do is prime

0:32:370:32:41

or sort of grease the pathway, as it were,

0:32:410:32:43

with electrical stimulation.

0:32:430:32:45

And as a consequence, enhance the sleep and memory benefit.

0:32:450:32:48

Electrodes are fitted onto Chris' head

0:32:500:32:53

so that Professor Walker can observe how much deep sleep he's getting.

0:32:530:32:57

The sleep stimulator seems to be working.

0:33:000:33:03

The monitor shows sharp movements in Chris' brain waves

0:33:030:33:07

which are the signatures of deep sleep and memory processing.

0:33:070:33:12

Now Professor Walker needs to know

0:33:120:33:15

whether this extra sleep has strengthened Chris' memory.

0:33:150:33:18

Now we're just going to perform the memory test.

0:33:180:33:22

Chris has to recognise faces from the earlier test.

0:33:220:33:26

If he remembers the face, or it seems to be familiar,

0:33:260:33:29

he has to click on it.

0:33:290:33:31

Then he has to recall the word which related to it.

0:33:310:33:35

The initial results of this experiment are very encouraging.

0:33:400:33:45

So what we're finding is that you need sleep after learning

0:33:450:33:48

to essentially cement those new memories.

0:33:480:33:51

And as a consequence, when people wake up the following morning,

0:33:510:33:54

those memories are more robust.

0:33:540:33:56

People have forgotten far less information across sleep

0:33:560:33:59

than they would if they'd remained awake.

0:33:590:34:02

It will be many years before the sleep stimulator is on the market.

0:34:020:34:06

By then, Professor Walker hopes enhancing deep sleep will be

0:34:060:34:10

a major weapon in the fight against Alzheimer's.

0:34:100:34:14

Can we, in those people who are fighting that battle with

0:34:140:34:17

Alzheimer's disease, improve sleep quality and try to bring back

0:34:170:34:22

online some degree of learning and memory function?

0:34:220:34:25

That's the first goal.

0:34:250:34:27

The second goal, however, is to regress the time-line back.

0:34:270:34:32

In other words, can we find ways to start to improve

0:34:320:34:35

sleep in people in their thirties, forties and fifties, to see if

0:34:350:34:40

we can actually move from a model of treatment to a model of prevention?

0:34:400:34:45

Until then, the research is beginning to show that

0:34:470:34:50

regular deep sleep throughout our lifetime

0:34:500:34:53

could lower our risk of developing the disease.

0:34:530:34:56

Sleeping is just one way we could change our lifestyle to

0:34:590:35:03

stave off Alzheimer's, but it's increasingly clear that what

0:35:030:35:07

we eat plays a role as well.

0:35:070:35:10

There is evidence that a diet should be rich in fish,

0:35:100:35:12

vegetables and olive oil,

0:35:120:35:15

but it's more important to have one main goal in mind.

0:35:150:35:20

In different studies, researchers have looked at different forms

0:35:200:35:23

of this diet, but what they all have in common is the ability

0:35:230:35:26

to protect the heart.

0:35:260:35:28

So, if there is a diet out there that is protective of the heart,

0:35:280:35:32

it may have that additional benefit of promoting

0:35:320:35:35

healthy ageing and reducing the risk of Alzheimer's disease.

0:35:350:35:38

Once the disease has started to develop,

0:35:380:35:41

choosing what to eat becomes much more complex.

0:35:410:35:45

Professor Richard Wurtman is a world expert on how nutrition

0:35:450:35:49

affects the development of the brain.

0:35:490:35:52

In a series of studies here in Boston, he started

0:35:520:35:55

looking at why people with Alzheimer's had so few synapses.

0:35:550:36:00

What the first slide shows is the part of a neuron, the part

0:36:000:36:03

of a neurocell that's involved in making new synapses and the

0:36:030:36:06

specific part are these little white dots you see running along the side.

0:36:060:36:10

Each one of those dots is very likely to become a new synapse.

0:36:100:36:14

Now, this is a similar part of the brain and what you can see is,

0:36:140:36:18

in Alzheimer's disease, you have many fewer of these white dots

0:36:180:36:21

and so you're producing many fewer synapses.

0:36:210:36:23

It had been found that the disease reduced existing synapses,

0:36:230:36:28

but that it also stopped new ones developing to replace them.

0:36:280:36:33

Professor Wurtman wanted to find out why this happened

0:36:330:36:36

and examined the role that nutrients, which help create

0:36:360:36:40

these new synapses, played in the development of the disease.

0:36:400:36:43

Alzheimer's patients quite generally have difficulty in smelling food

0:36:430:36:47

and in tasting food,

0:36:470:36:48

And they also have difficulty in absorbing most nutrients

0:36:480:36:51

and in producing some of the nutrients in their own livers.

0:36:510:36:54

So, they start out with nutritional deficiencies.

0:36:540:36:57

His studies have discovered three nutrients which are essential

0:37:020:37:06

for making new synapses to replace those destroyed by the disease.

0:37:060:37:10

They are choline,

0:37:100:37:12

uridine,

0:37:120:37:14

and docosahexaenoic acid, known as DHA.

0:37:140:37:17

Here you see an excellent source of DHA in the diet.

0:37:190:37:22

This is a fish. It happens to be a salmon.

0:37:220:37:25

Patients with Alzheimer's disease do have some

0:37:250:37:27

difficulty in absorbing DHA.

0:37:270:37:29

Choline is present in abundant quantities within egg yolks, OK?

0:37:300:37:34

And if you have three eggs and three egg yolks,

0:37:340:37:37

then you're doing pretty well in terms of getting choline.

0:37:370:37:40

And again, Alzheimer's patients have some difficulty in absorbing it.

0:37:400:37:44

The third, uridine, can't be obtained from food,

0:37:440:37:47

but is normally created in the liver,

0:37:470:37:49

something people with Alzheimer's have difficulty doing.

0:37:490:37:53

The professor's work reveals that an Alzheimer's brain could benefit

0:37:530:37:57

if more of these nutrients could be absorbed to grow new synapses.

0:37:570:38:02

A new supplement has been created

0:38:020:38:04

which provides doses of these nutrients.

0:38:040:38:07

There have been two large-scale clinical trials

0:38:070:38:10

and in both trials it significantly improved memory function.

0:38:100:38:13

It also improved the connectedness between different

0:38:130:38:16

parts of the brain and that's critically important in people

0:38:160:38:19

with early Alzheimer's disease.

0:38:190:38:22

Although the trials showed the supplement helps early-stage

0:38:220:38:25

Alzheimer's patients,

0:38:250:38:26

people who have the more advanced stage of the disease do not benefit.

0:38:260:38:31

Across the world, researchers are searching for ways

0:38:400:38:44

not just of renewing the synapses,

0:38:440:38:46

but of improving the functioning of the brain in general.

0:38:460:38:50

Millions of people practice cognitive exercises,

0:38:530:38:57

known as brain-training.

0:38:570:38:59

Cognitive exercises are probably helpful for all of us.

0:38:590:39:02

It's good for us to keep our brains working and we know that

0:39:020:39:05

if you engage in a lot of cognitive activity,

0:39:050:39:07

it can help to reduce your risk

0:39:070:39:10

of developing cognitive impairment and dementia.

0:39:100:39:13

However, we've systematically reviewed the evidence,

0:39:130:39:16

the research evidence, about brain-training people with

0:39:160:39:18

Alzheimer's disease and, unfortunately, we haven't been

0:39:180:39:21

able to find any strong evidence that this is beneficial.

0:39:210:39:24

Alzheimer's patients need to concentrate on much more

0:39:300:39:34

frequent and routine ways of training their brains.

0:39:340:39:38

This could help people like Gareth Hulston,

0:39:380:39:41

who lives in North Wales.

0:39:410:39:43

He's 68 years old

0:39:430:39:45

and was diagnosed with Alzheimer's a year ago.

0:39:450:39:48

He's surrounded by reminders of a rich and full life,

0:39:490:39:53

but gradually, he's forgetting their significance.

0:39:530:39:56

His daughter, Virginia, is doing her best to stimulate his memory,

0:39:560:40:00

asking him what he's been up to.

0:40:000:40:02

What did you do on Saturday, Dad?

0:40:020:40:04

Hang on....

0:40:070:40:09

What did I do on Saturday?

0:40:110:40:13

Can't remember.

0:40:170:40:19

But fortunately for Gareth, he's been chosen to take part

0:40:190:40:23

in an important new trial run by Professor Linda Clare.

0:40:230:40:27

She hopes it will teach him

0:40:270:40:29

to focus on improving everyday tasks which are causing him problems

0:40:290:40:33

and, in the process, engage his brain many times every day.

0:40:330:40:37

What we try to do is get them to think with us

0:40:370:40:40

about all of the different steps involved in the activity

0:40:400:40:42

that they want to manage better.

0:40:420:40:44

And then to really engage their brain in

0:40:440:40:47

figuring out where the difficulties are coming in that process.

0:40:470:40:50

And we work with them to develop strategies that they can apply

0:40:500:40:53

at the different stages so that they may manage that activity better.

0:40:530:40:57

Therapist Sue Evans is visiting Gareth to find out

0:40:570:41:01

which everyday skills he wants to improve.

0:41:010:41:04

-Hi, Sue. How are you? Come on in.

-Nice to see you, Gareth.

0:41:040:41:09

At the moment, he's having problems with cooking.

0:41:090:41:13

Right. Are these the eggs, are they?

0:41:130:41:16

Watch, don't, don't. You need a cloth, they're hot.

0:41:220:41:25

How are you today, then, Gareth?

0:41:250:41:28

Not too bad. I keep going, don't I?

0:41:280:41:30

-Take a pew.

-OK, I will do.

0:41:300:41:33

I'm just going to sit and watch and listen to you

0:41:330:41:35

and Virginia for a bit, OK?

0:41:350:41:37

Sue observes him for 30 minutes to see how the disease is

0:41:370:41:40

affecting his planning and concentration.

0:41:400:41:43

What are you going to have for dinner tonight?

0:41:430:41:45

Haven't a clue, not a clue.

0:41:450:41:47

You not planned anything?

0:41:470:41:49

No, I might go to see Bill.

0:41:490:41:51

Can you smell anything, Dad?

0:41:520:41:54

No, my smell's gone, hasn't it? I can't smell at all.

0:41:540:41:58

What did you put on before?

0:41:580:42:00

Oh, I put some eggs on to boil.

0:42:000:42:03

Yeah, so what's burning?

0:42:030:42:04

Do you want me to go and have a look?

0:42:040:42:07

I would, I'd go and have a look.

0:42:070:42:09

Just in time.

0:42:140:42:15

What's burning, Dad?

0:42:150:42:17

Hang on, what's in the oven?

0:42:170:42:18

Oh, you're joking, Virginia.

0:42:210:42:23

Oh, they're ruined.

0:42:230:42:25

They're absolutely burnt to a cinder.

0:42:270:42:30

Sue wants to help Gareth work out a series of steps which

0:42:300:42:34

will become part of his routine and stop him burning his meals.

0:42:340:42:38

-So you told me there was a pizza in the fridge.

-Yes.

0:42:380:42:40

So, do you want to get it out?

0:42:400:42:43

Yeah, all right.

0:42:430:42:45

Let's have a look.

0:42:450:42:46

So, if you're going to cook this one, let's have a look and see.

0:42:460:42:49

What would you find out?

0:42:490:42:50

Eight to ten minutes here.

0:42:500:42:52

Yeah? So, come over here and write that information down, yeah?

0:42:520:42:58

So you'd write pizza.

0:42:580:43:00

OK. And what time is it going to be ready?

0:43:030:43:05

And then the next thing I need you to do is set the timer.

0:43:080:43:11

So the reason I'm getting you to write all this down

0:43:110:43:14

is that I'm making you think about it more, which one -

0:43:140:43:17

it means it's gone through more processes in your brain,

0:43:170:43:20

because you've had to read it, think about it and then write it.

0:43:200:43:24

But also, this also works as a back up.

0:43:240:43:27

She hopes that by thinking through these steps several times a day,

0:43:280:43:32

Gareth's planning abilities will improve.

0:43:320:43:35

Sue also wants to work on his semantic memory -

0:43:350:43:38

his ability to remember facts.

0:43:380:43:40

His challenge is to remember the names of his grandchildren.

0:43:400:43:44

Who's that?

0:43:440:43:46

I cannot remember.

0:43:460:43:47

-Rachel.

-Rachel?

0:43:470:43:49

So, Rachel.

0:43:490:43:50

She's the boss.

0:43:500:43:51

She's the boss, that doesn't surprise me.

0:43:510:43:54

Sue has one simple recommendation.

0:43:540:43:57

-Maybe that's a project to do to get an up-to-date photo of her.

-Yeah.

0:43:570:44:01

By having that photo in your hand,

0:44:010:44:04

you're able to build up more of an image of them

0:44:040:44:07

and then hopefully what we'd be aiming for is that you'd be able to

0:44:070:44:11

build up that image of them without needing the photo in your hand.

0:44:110:44:15

Sue returns every week to ensure Gareth is incorporating these

0:44:150:44:19

techniques into his daily routine.

0:44:190:44:21

Three months later, now it's time for Sue to find out

0:44:250:44:28

whether Gareth's planning abilities and memory have improved.

0:44:280:44:33

-Hiya, Sue!

-Hi, Gareth.

0:44:330:44:35

-Come on in.

-How are you? Nice to see you.

0:44:350:44:38

First up, can he remember not to burn his food?

0:44:380:44:41

OK, Gareth, so you're going to show me how you're doing

0:44:410:44:44

the cooking now, now you've been using the strategies for a bit?

0:44:440:44:48

He's been putting them in action, helped by a new hi-tech oven.

0:44:480:44:52

Right, all you do then is get that from there.

0:44:520:44:57

Now cooking instructions, 20 to 25 minutes.

0:45:000:45:06

Gareth has become so good at planning this task that he

0:45:060:45:08

no longer needs the white board.

0:45:080:45:11

He just uses the timer as a prompt.

0:45:110:45:13

He sets it for 20 minutes.

0:45:130:45:15

Right. And this is what I do, as a rule.

0:45:150:45:18

This is where I usually put it, on there, and I usually take this seat.

0:45:180:45:23

So, Gareth, have you managed to get an up-to-date picture of Rachel?

0:45:230:45:26

That was one of the jobs I gave you last time, wasn't it?

0:45:260:45:29

Yes, I got the photograph. There she is.

0:45:290:45:31

There she is. Oh, that's a nice one.

0:45:310:45:33

-At her right age.

-Yeah.

-Much better.

0:45:330:45:36

TIMER RINGS

0:45:360:45:38

Oh!

0:45:380:45:40

Go on, then.

0:45:400:45:41

The plan has worked.

0:45:430:45:45

Gareth appears to have retrained his brain to connect

0:45:450:45:47

the sound of the timer with the cooking.

0:45:470:45:50

Right.

0:45:510:45:52

-So, this turns itself off too, then?

-Yeah.

-Yeah?

0:45:520:45:56

So, no risk of burning any more.

0:45:560:45:58

They look good. So they're done?

0:45:590:46:01

They are absolutely ready, yeah.

0:46:010:46:03

Yeah? Excellent.

0:46:030:46:04

And now for the ultimate test.

0:46:060:46:09

Has his training improved his semantic memory?

0:46:090:46:12

-Hiya, Rache!

-Hiya, Grandad.

0:46:180:46:21

Come on in.

0:46:210:46:22

She's my grand-daughter, my Rachey-wachey.

0:46:240:46:27

HE LAUGHS HAPPILY

0:46:270:46:31

Oh, I'll never give in. I'll never ever give in.

0:46:310:46:34

Might put me in my box, but I'll never...I'll never give in.

0:46:340:46:40

I do believe I've improved tremendously.

0:46:400:46:42

We'll go from this side across, yeah, and you can tell me

0:46:420:46:45

who everyone is now.

0:46:450:46:46

-That's Nathan.

-That's Nathan.

-Holly...

0:46:460:46:49

These simple steps help people like Gareth to manage their lives better,

0:46:490:46:54

but they can also improve the functioning of their brains.

0:46:540:46:58

Dwayney, the decorator.

0:46:580:47:00

People who had had the cognitive rehabilitation programme

0:47:000:47:02

showed greater activation when they were doing a memory task

0:47:020:47:05

in certain brain areas, particularly the bilateral frontal areas.

0:47:050:47:10

Whereas people in the control group who hadn't had the programme

0:47:100:47:13

showed reduced activation in those areas.

0:47:130:47:16

We tentatively suggested that this might reflect

0:47:160:47:20

some improvement in functioning in those areas of the brain.

0:47:200:47:23

And, of course, that relates very much

0:47:230:47:24

to the way the intervention works,

0:47:240:47:26

where we're asking people to think about strategies

0:47:260:47:29

and engage in particular strategies to manage everyday activities

0:47:290:47:32

that help them to manage those better.

0:47:320:47:33

Simple lifestyle changes seem to re-train

0:47:370:47:39

and strengthen the functioning of the brain in people

0:47:390:47:42

who are suffering from early-stage Alzheimer's.

0:47:420:47:45

But in this new era of research,

0:47:460:47:49

there is a much more dramatic ambition.

0:47:490:47:52

This is a really exciting time for patients with Alzheimer's disease

0:47:520:47:56

because we're starting to see trials that are starting

0:47:560:47:59

to show evidence of efficacy.

0:47:590:48:00

And I think there's a lot of excitement now,

0:48:000:48:03

because there's some new data that looks very promising.

0:48:030:48:06

This new data has launched worldwide drugs trials.

0:48:060:48:11

One is taking place in Colombia.

0:48:110:48:13

Here, the Alzheimer's gene mutation, which afflicts families like Flor's,

0:48:180:48:23

offers a rare opportunity for research.

0:48:230:48:26

In these families, the gene causes the amyloid to start building up

0:48:260:48:31

in people as young as 30 and symptoms appear at 45,

0:48:310:48:35

as has happened with Flor's sister Olga.

0:48:350:48:38

Researchers want to find out if a drug can interrupt its progress.

0:48:380:48:44

The prospect that Flor might have the early stages of the disease

0:48:440:48:48

makes her a valuable participant.

0:48:480:48:50

Every two weeks, Flor goes for physical and cognitive tests

0:49:200:49:24

and she's given an injection which could be the brand-new

0:49:240:49:27

Alzheimer's drug crenezumab or it could be a placebo.

0:49:270:49:31

Crenezumab is an anti-amyloid treatment that had several

0:49:330:49:36

characteristics we thought were especially

0:49:360:49:39

suitable for prevention trials.

0:49:390:49:41

It seemed to attack different forms of amyloid

0:49:410:49:43

and there was a suggestion that it could reduce amyloid and

0:49:430:49:47

might have a role if it was started in people at an earlier stage.

0:49:470:49:52

IN SPANISH:

0:49:520:49:54

For Dr Lopera, the trial offers a new future.

0:49:580:50:02

IN SPANISH:

0:50:020:50:04

Five one way.

0:50:150:50:16

Meanwhile, 4,000km away in New England, Neil Corkery

0:50:160:50:21

is part of another trial which already has promising early results.

0:50:210:50:26

Ten years ago, the 75-year-old former head teacher

0:50:280:50:31

and local politician first noticed he had the symptoms of Alzheimer's.

0:50:310:50:37

We were going to an event for one of the state officials who was

0:50:370:50:41

leaving and the Governor was supposed to speak.

0:50:410:50:44

So he was late and they said, "Would you say a few words?"

0:50:440:50:47

And I said, "Sure, I'll be glad to." And I got up and I started

0:50:470:50:50

and I was fine and then I got to a point,

0:50:500:50:53

I blanked out on a word and that's when I went for some tests.

0:50:530:50:57

Doctors scanned his brain and diagnosed him with Alzheimer's.

0:50:570:51:02

The news was devastating for Neil and his wife, Maureen.

0:51:020:51:06

Initially - I've never told Maureen this - I did things like put

0:51:060:51:10

music on that they could use when I, when they have the funeral.

0:51:100:51:15

Like Glen...

0:51:150:51:17

who's, Glen, Glen Campbell, who's a noted singer.

0:51:170:51:23

He has, he's got a song that they had him sing

0:51:230:51:26

and it's just a beautiful song.

0:51:260:51:29

# I'm still here but yet I'm gone... #

0:51:290:51:34

So I was kind of romancing the kind of negative side of it,

0:51:350:51:40

I guess, but I've been through that, I hope, you know.

0:51:400:51:44

I think we both felt depressed after the diagnosis,

0:51:440:51:49

because you know there's no cure.

0:51:490:51:52

The future for the Corkerys looked bleak.

0:51:520:51:55

Luckily for them,

0:51:550:51:56

tests had just started on a new drug to fight Alzheimer's.

0:51:560:52:00

In 2014, the man behind the drug was on the way to his office

0:52:020:52:07

when his chief executive called with the results of its Phase 1 trial.

0:52:070:52:11

I was driving down the street.

0:52:110:52:13

When he started to tell me the results, I had to pull over,

0:52:130:52:15

because they were so exciting.

0:52:150:52:17

And he was telling me

0:52:170:52:18

that the drug had unexpectedly shown an effect on cognitive decline.

0:52:180:52:23

Our drug was slowing cognitive decline in patients

0:52:230:52:26

with Alzheimer's disease.

0:52:260:52:28

I'm glad I pulled over, because I was so excited

0:52:280:52:31

and I...I was smiling from ear to ear.

0:52:310:52:34

The drug, called aducanumab, was what everyone had been hoping for.

0:52:340:52:40

The results sent share prices

0:52:400:52:41

in the pharmaceutical company Biogen rocketing.

0:52:410:52:45

The trial showed that the drug was having a remarkable

0:52:460:52:49

impact on the brains of people with Alzheimer's.

0:52:490:52:52

So what we're looking at here is a slice of a human brain

0:52:520:52:55

in the living patient with Alzheimer's disease.

0:52:550:52:57

And what we see here is a red colour and yellow.

0:52:570:53:01

And the red colour shows where the amyloid plaques are in the brain.

0:53:010:53:04

And the more red it is, the more plaque there is.

0:53:040:53:08

This shows what happens after treatment with our drug.

0:53:100:53:13

We see that the redness has been reduced and that

0:53:130:53:16

means that the amyloid plaques have been removed from this brain.

0:53:160:53:21

The scan on the right shows just how effective

0:53:210:53:24

the drug has been in removing amyloid plaque from the brain,

0:53:240:53:28

but a major complication has now been discovered.

0:53:280:53:31

The main side effect that we saw with this drug in the clinical trial

0:53:310:53:35

was a thing called ARIA.

0:53:350:53:37

And what we see here is a picture of ARIA.

0:53:370:53:40

And what we see is a whiteness here in this...in the brain,

0:53:400:53:43

which signifies oedema or swelling in the brain.

0:53:430:53:46

And that's not a good thing,

0:53:460:53:48

because the brain is in an enclosed space

0:53:480:53:50

and swelling can be harmful to patients.

0:53:500:53:54

Researchers hope to stop the swelling by initially giving

0:53:540:53:57

a low dose of the drug and then gradually increasing it.

0:53:570:54:01

Extensive phase III trials

0:54:010:54:03

are being rolled out across Europe and America.

0:54:030:54:06

There is even a possibility that the drug will combat the tau tangles,

0:54:060:54:10

that other great hallmark of Alzheimer's disease.

0:54:100:54:13

But the results won't be known for four years.

0:54:130:54:16

-How are you today?

-Very good.

0:54:160:54:18

Neil Corkery is now participating in the trial.

0:54:180:54:22

He doesn't know whether he's on a placebo or the drug,

0:54:220:54:25

but taking part has made all the difference.

0:54:250:54:28

Recently, he was even able to speak off the cuff at his son's wedding.

0:54:290:54:34

I was like my old self. I really...

0:54:340:54:37

Yeah, it was extemporaneous

0:54:370:54:39

and there wasn't any rehearsal or written words or anything.

0:54:390:54:43

He just got up and he spoke and it flowed.

0:54:430:54:47

It was nice, it was really nice.

0:54:470:54:49

She's been by me all the time.

0:54:490:54:51

She's, she...

0:54:510:54:53

She knows what's right.

0:54:530:54:55

It has made me feel better, yeah, absolutely.

0:54:550:54:58

I mean, I don't know what else to attribute it to,

0:54:580:55:00

you know, unless it's a miracle I'm unaware of.

0:55:000:55:03

Neil is convinced he is benefiting from the drug trial,

0:55:030:55:07

although it could be the famous placebo effect.

0:55:070:55:09

TANGO MUSIC PLAYS

0:55:090:55:13

For Flor, who's taking part in the Colombia trial,

0:55:140:55:18

the curse of Alzheimer's which has hung over her family for

0:55:180:55:21

so long could at last be lifted.

0:55:210:55:24

IN SPANISH:

0:55:260:55:28

The first results from this trial

0:55:370:55:39

will also become available in around four years.

0:55:390:55:42

These trials, and others around the world,

0:55:460:55:49

are bringing hope to millions.

0:55:490:55:52

We believe it marks the dawn of a new era

0:55:530:55:56

in Alzheimer's-prevention research.

0:55:560:55:59

And that gives us now the opportunity to rapidly evaluate

0:55:590:56:03

the range of promising but unproven prevention therapies.

0:56:030:56:07

And maybe, just maybe, find and support the approval

0:56:070:56:11

of effective prevention therapies within the next ten years.

0:56:110:56:15

There's a lot of hope for Alzheimer's patients.

0:56:160:56:19

We're in the final stages of clinical trials with a drug

0:56:190:56:22

that looks very promising.

0:56:220:56:23

We can remove the amyloid from the brains of patients

0:56:230:56:26

with Alzheimer's disease.

0:56:260:56:27

My hope is that if we treat early enough, we may stave off Alzheimer's

0:56:270:56:32

disease completely and we may never have to worry about it again.

0:56:320:56:35

Up until now, a treatment for Alzheimer's has eluded scientists.

0:56:370:56:42

We can all make changes to our lifestyles and help

0:56:420:56:46

stave off the disease, like eating well and getting enough sleep.

0:56:460:56:50

But innovative scanning techniques and a new generation of drugs

0:56:500:56:55

are giving people with Alzheimer's, and those at risk of developing it,

0:56:550:56:59

new hope that they will hold on to their memories and their lives.

0:56:590:57:04

# I'm still here but yet I'm gone

0:57:060:57:11

# I don't play guitar or sing my song

0:57:130:57:18

# It never defined who I am

0:57:210:57:25

# The man that loves you till the end

0:57:280:57:33

# You're the last person I will love

0:57:370:57:41

# You're the last face I will recall

0:57:440:57:49

# And best of all

0:57:490:57:52

# I'm not gonna miss you

0:57:560:57:59

# I'm not gonna miss you

0:58:030:58:07

# I'm never gonna hold you like I did

0:58:140:58:18

# Or say "I love you" to the kids

0:58:210:58:26

# You're never gonna see it in my eyes. #

0:58:290:58:34

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