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Experiment could show whether insomnia raises your risk of Alzheimer’s

Does insomnia raise your risk of Alzheimer’s? Scientists have feared for years that lack of sleep can be linked to dementia, now a ground-breaking experiment could uncover the truth

  • The Mail on Sunday was granted exclusive access inside cutting-edge sleep lab
  • Scientists at the University of East Anglia hosting 40 participants for new study
  • Deputy Health Editor Eve Simmons describes her experiences of taking the test

These days, I don’t sleep nearly as well as I used to. And I certainly can’t shrug off the effects of a restless night as easily as I once did. But aside from being annoying, I’m often left worrying after hours of tossing and turning – could my disturbed sleep be a sign of something more sinister? Perhaps it is an unfortunate consequences of ageing.

Or, as the latest scientific findings suggest, it may in fact be a sign that my brain is not as healthy as it could be. It is well known that those with neurological, degenerative diseases such as Alzheimer’s sleep badly.

It has long been believed that lifetime insomniacs are much more likely to suffer irreversible brain damage.

Mail on Sunday Deputy Health Editor Eve Simmons takes part in a cutting-edge new experiment at the University of East Anglia (UEA). She is pictured here with Dr Michael Mosley

Eve’s brainwaves were monitored during the test. She has 18 pin-sized electrodes dotted over her crown, chin and forehead. These are attached to long wires that are held in place with an oily glue (she is pictured here alongside Dr Michael Mosley, right, and Dr Alpar Lazar)

Some studies estimate that the lifetime risk of dementia rockets by a third among those who suffer with poor sleep on a long-term basis.

We also know that those who pop sleeping pills regularly are more likely to suffer cognitive decline in later life.

There’s no doubt that poor sleep and Alzheimer’s go hand in hand. But so far, science has failed to reveal the cause of this relationship.

What comes first? Does a build-up of sleepless nights cause the brain to rot? Or are those at high risk of Alzheimer’s more likely to struggle with sleep?

Now, a pioneering British study aims to find out. The Mail on Sunday has been granted exclusive access inside a cutting-edge sleep laboratory at the University of East Anglia (UEA).

Over the next six weeks, scientists will host 40 participants (well, 41, counting Mail on Sunday Deputy Health Editor Eve Simmons, who was also brave enough to volunteer her brain for the experiment).

After being genetically tested to determine their risk of Alzheimer’s disease – the most common form of dementia – they will be divided into two groups.

One group will be kept awake for 40 hours – roughly two days – and the others will be less sleep-deprived and allowed short naps.

As Eve writes on these pages, taking part in these sorts of experiments is not much fun. Not only do you have to fight the powerful urge to sleep, but throughout the experiment our participants will be subjected to a series of challenging tests to assess things such as memory, balance, co-ordination and focus.

Eve had to stay awake until 3am, unlike the real-life participants kept awake for two nights on the trot

The prediction, according to Dr Alpar Lazar from the University’s School of Health Sciences, is that those at the highest genetic risk of dementia will do significantly worse in the tests than others when sleep-deprived.

He explains: ‘Studies show that people at high genetic risk of Alzheimer’s struggle more with sleep. It’s also been shown that a combination of poor sleep and high genetic risk for Alzheimer’s makes you more likely to develop cognitive problems, as well as developing dementia, compared to others without those vulnerabilities.’

Ultimately, this could help doctors identify whether specific problems with sleeping, or reported difficulties in performing everyday tasks when tired, might identify dementia at an early stage.

COULD LIGHT THERAPY HELP TREAT ALZHEIMER’S?

The UEA experiment will go further: some of the volunteers will be allowed to nap for an hour, at specific times.

The body’s sleep-wake cycle, or circadian rhythm, is governed by the release of certain hormones and other body chemicals. Some, like noradrenaline, are released when the eyes sense daylight, and they help to keep us alert.

EVE SIMMONS reveals what happened when she bravely took part in the experiment 

It’s 2.05am and I’m staring hopelessly at a pair of old, crinkly feet. Of the 20 ‘memorable’ images flashing up on screen, it’s the only one my brain has registered.

I’m midway through a memory test designed to measure the capacity of my sleep-deprived brain.

I’ve now been awake for a solid 20 hours which means, thankfully, there’s just 55 minutes left of my experiment.

‘The longer I stayed awake, the more my brain went haywire’, writes Eve Simmons

It’s at about this point that signs of a genetic vulnerability would begin to show.

If I were a carrier of the genetic variety that makes you 12 times more likely to get dementia, I could even experience psychiatric disturbances such as hallucinations or panic attacks.

Thankfully none of the above has set in… yet.

I’m no scientist, but intuition tells me I’m not performing well in these tests.

For one, I’m distracted by the constant itch of 18 pin-sized electrodes dotted over my crown, chin and forehead.

They are monitoring my brainwaves, and attached to long wires that are held in place with an oily glue which has formed matted clumps in my hair, making it stick up.

As a journalist previewing the University of East Anglia’s sleep experiment, I’m only staying awake until 3am, unlike the real-life participants kept awake for two nights on the trot.

I didn’t think this would be difficult. In fact, I jumped at the chance to spend a night wide awake for the sake of science.

But without the usual distractions that might keep me up that late – at a party, for instance – it was torture. When I arrived at 5pm, I did the first series of tests. These were to be repeated later in the night when sleep deprivation kicked in.

Words flashed up on a screen, some of which were nonsense, and I had to pick out the ‘non-words’ using a keyboard. I was shown one sequence of pictures, followed by another, and asked to say whether, the second time round, I’d seen any of them before.

Another test involved balancing on a platform with my eyes closed – which is harder than it sounds. I’m then asked to hover my hand over a button without touching it. At 5pm, I barely wobbled. But now, nine hours later, my legs were trembling, swaying sideways.

‘Be careful with this one,’ Professor Lazar, who runs the experiment, warns. ‘At your level of sleep deprivation, there’s a risk of sudden fall and bone breakages.’

As his first-ever participant, I’m not filled with confidence by Dr Lazar’s words.

The sleepiness set in at 10pm, thanks to the dimmed, artificial light and cool 18C temperature in my ‘bedroom’, designed to make me feel sleepy. I was advised to keep my distance from the bed, and the large, ornate armchair wasn’t as comfortable as it looked.

I passed the time watching things on Netflix, struggling to keep my eyes open.

At about midnight, I began to imagine I could hear a whirring noise which disappeared when Dr Lazar returned for my final round of tests – it seems I was desperate for some human contact.

When the tests are over, at 2.50am, it’s time to tuck me in.

I leap under the duvet while research assistants plug my dangling wires into a hand-held monitor. The device will transmit my brain activity on to Dr Lazar’s computer screen.

According to my brain scan, it took precisely three-and-a-half minutes for me to fall asleep.

‘This is very quick, suggesting you were very tired,’ Dr Lazar explains the next morning.

He also tells me that a third of my sleep was the intensive, deep kind. This level is above average and considered a sign of exhaustion.

A week later, I’m given the results of my cognitive tests.

At 7.30pm, I’d scored 96 per cent on the memory tests, with only three errors.

At 2am this rocketed four-fold – I made 12 mistakes.

I chose not to have the Alzheimer’s gene test prior to the experiment. I really didn’t want to know either way.

But taking part did make me realise why I enjoy nothing more than an early night.

Others, such as melatonin, are released when it gets dark, and slow down the body’s processes, making us sleepy. In people with dementia, the release of these chemicals is believed to be disrupted. By allowing the volunteers to nap, the scientists will be able to track the volunteers’ sleep-wake cycle – albeit artificially induced – a number of times.

In theory, those with the dementia gene may display abnormalities during these cycles, compared to those without the gene.

Ultimately, this may herald a new way to treat the disease, says Dr Lazar. He explains: ‘Regulating the circadian rhythm has been shown to slow the progression of other neurodegenerative diseases such as Huntingdon’s disease in animals. Using light is a powerful way to do this. It is possible that these interventions could work in a similar way for dementia.’

WOULD YOU WANT TO KNOW IF YOU’LL GET DEMENTIA?

As I mentioned, all the volunteers must take the genetic test which looks at variants of a gene linked to Alzheimer’s risk called APOE. About five per cent of the population carry two copies of the E4 variant of the APOE gene, which makes them 15 times more likely to develop Alzheimer’s later in life. Understandably, not all participants wish to know their results.

For the purposes of the experiment, neither the participants nor the research assistants are informed of their genetic status to be sure it doesn’t impact the results of the study.

The tests have been around for a while and, as I did want to find out my risk of Alzheimer’s, I’ve already had myself independently tested by a private genetic-testing company called 23andme.

I paid a small fee and supplied a swab of the inside of my mouth which I then posted off to the company.

Thankfully, I had no copies of the E4 variant, which means my risk of developing Alzheimer’s by the age of 75 is less than two per cent.

Carrying one copy of the variant raises the risk to about six per cent. Two copies sees risk climb to 28 per cent under the age of 75, and this doubles to 60 per cent once you reach 85. So I’m lucky.

But for tens of thousands of Britons, the odds aren’t so promising. With any luck, the results of this experiment – expected this time next year – will show that even these people needn’t be defined by their genetics.

WHAT HAPPENS WHEN WE ARE ASLEEP?

I didn’t join Eve in her sleep-deprivation experiment – I’ve done a few myself over the years and that’s enough to last a lifetime.

A couple of years ago I took part in an experiment to measure the impact of sleep-deprivation on concentration and mood.

For three nights I slept just four hours a night, staying awake till 3am, then waking up at 7am.

I thought I’d be able to get lots done with those extra four hours a day, but instead I just watched terrible films and stared at the clock until it was time for bed.

Each day I took part in simulated driving tests and psychological surveys.

Some of my fellow volunteers claimed to feel fine, but the tests revealed otherwise.

Not only were our reaction times shot to blazes, but we also all showed signs of increased anxiety, depression and stress.

Remarkably, just a single good night’s sleep was enough to improve all these outcomes significantly.

Another particularly uncomfortable experiment involved me wearing a tight cap that measured brainwave activity, heart rate and eye muscle movement, called an electroencephalograph.

I was allowed to take the kit home and sleep in my own bed. That night, feeling slightly ridiculous, I went to bed at 11pm and soon fell asleep. According to the electroencephalograph reading I fell asleep within a minute of turning off the lights. I’d quickly entered what’s known as stage one sleep: a light stage where you can still be easily woken.

Next, I entered stage two – a fairly light sleep but with a slowed heart rate. This phase can be identified clearly on brain scans as a series of exaggerated spikes.

Soon afterwards, brainwaves slow and you slip into deeper sleep, or stages three and four.

Eye movements stop and the brain’s electrical activity slows even further.

It is this stage of sleep that is often considered the most important, as it is a stage when your body conducts essential repairs on tissues, bones and nerves, produces hormones that spark growth and boosts cells of your immune system.

And when it comes to maintaining brain health, deep sleep is vital.

HOW DEEP SLEEP CAN PROTECT AGAINST DEMENTIA

Although scientists have not yet concluded that a lack of deep sleep causes dementia, there’s no doubt it affects the memory dramatically. Researchers believe that during deep sleep, memories from the day – short-term memories – are sorted and moved into long-term storage, allowing more space for short-term memories the following day.

Without ample deep sleep, these memories will be lost. In order to make it into our long-term stores, they need to be consolidated within 24 hours of being formed.

We know this because research has shown it to be the case: in one study, students who sat up all night cramming performed 40 per cent worse than their contemporaries.

Deep sleep is also crucial for maintaining the glymphatic system – which is responsible for ‘cleaning’ the brain – which is believed to play a role in protecting against dementia. These purple-coloured ‘lymphatic’ blood cells at the back of the skull transport fluid through the brain tissue and wash away excess, naturally occurring proteins.These include the build-up of beta amyloid proteins and tau – tangled protein in the nerve cells – linked to Alzheimer’s.

Two recent studies, published in the journal Science Translational Medicine And Science, found long-term poor sleepers to have concerningly high levels of tau – used as a telltale sign of early-stage dementia. Another US study published this month found that just one night of sleep deprivation increased the presence of beta amyloid proteins by five per cent.

Reassuringly, the electroencephalograph showed I was getting about an hour of deep sleep each night, considered a perfectly normal amount.

As I write, at the UEA Sleep Lab their second participant will be waking up from their second nap of the evening, to be prepared for another barrage of gruelling tests before being sent back to sleep again.

Their results may unlock further doors in the search for answers about the brain illness that, if trends continue, will affect more than one million Britons by 2025.

And, ultimately, with more understanding, we might find an effective treatment – for, at present, there is little hope.

To be a fly on the wall would be fascinating. But I must admit, this time, I’m glad I’m not the guinea pig.

What’s the difference between a sprain and a strain? 

A sprain occurs when the tough bands of fibrous tissue that connect one bone to another within a joint, known as the ligaments, are stretched too far or torn. It commonly happens in the ankle or wrist during activity, and can be identified by the presence of rapid swelling and intense pain.

A strain occurs when the muscle or tendon – the tissue that attaches muscle to a bone – is torn or stretched too severely.

It usually happens in the hamstring or back and may lead to bruising and significant loss of muscle function. Both strains and sprains can be treated at home with a cold compress to reduce the swelling, and by resting.

Ask a stupid question: Why do babies’ eyes often change from blue to brown?   

‘This phenomenon is more common in Caucasian babies,’ says consultant eye surgeon Allon Barsam, of Ophthalmic Consultants of London.

‘Levels of melanin, the pigment which gives eyes their colour, increase gradually after birth, leading to baby-blue eyes turning green or hazel or brown.’

We inherit a mixture of eye colour from our parents: the genes for darker colours tend to dominate, so brown tends to win out over green, and green tends to win out over blue.

Mr Barsam adds: ‘By about the age of one, you will know the child’s definitive eye colour.’

Mental-health campaigner Claire Eastham

Blog me better  

The blog: allmadhere.co.uk

The blogger: Award-winning writer and mental-health campaigner Claire Eastham who has suffered with social anxiety disorder since she was a teenager and now fights for support for mental-health disorders.

What’s it all about?

Drawing on her experiences of crippling anxiety and panic attacks, Claire, 30, offers evidence-based advice on dealing with the day-to-day difficulties that come with a mental illness. Her YouTube videos provide a window into her life, giving comfort to other sufferers.

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