Category: Dementia

There are around 5.5 million Americans living with Alzheimer’s and deaths have almost doubled in two decades.

Exercise could be the lifesaving ingredient that prevents Alzheimer’s disease, new research finds.

Higher levels of fitness were linked to less deterioration of critical nerve fibers in the brain, the so-called ‘white matter’.

The brain’s white matter is the bundle of nerve fibers the neurons use to communicate with each other.

People with lower levels of fitness had weaker white matter and lower brain function.

Dr Kan Ding, the study’s first author, said:

“This research supports the hypothesis that improving people’s fitness may improve their brain health and slow down the aging process.”

The scientists measured people’s cardiorespiratory fitness along with carrying out brain scans.

Dr Rong Zhang, study co-author, said:

“Evidence suggests that what is bad for your heart is bad for your brain.

We need studies like this to find out how the two are intertwined and hopefully find the right formula to help prevent Alzheimer’s disease.”

Further research at the O’Donnell Brain Institute at The University of Texas Southwestern Medical Center is now examining how much exercise works and whether it is ever too late.

The study will also look at the effects of cholesterol levels and blood pressure on preserving brain function.

Dr Ding said:

“A lot of work remains to better understand and treat dementia.

But, eventually, the hope is that our studies will convince people to exercise more.”

The study was published in the journal Journal of Alzheimer’s Disease (Ding et al., 2017).

The first time scientists have been able to completely clear the brain of Alzheimer’s-related protein tangles.

Alzheimer’s has been reversed in mice for the first time, raising the hopes of a drug to combat the disease.

Decreasing the levels of a key enzyme — called BACE1 — reduced the levels of amyloid plaques, which are linked to Alzheimer’s.

The mice’s brains were eventually completely free of these tangles and their cognition improved.

This is the first time scientists have been able to clear the brain of these protein tangles.

It is possible a drug could be developed to help target this enzyme.

Professor Riquiang Yan, who led the study, said:

“To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer’s disease mouse models.”

For the study, the scientists created mice that produce lower levels of the BACE1 protein over time.

The mice were also engineered to develop Alzheimer’s.

After developing Alzheimer’s at 75 days old, these mice were then clear of the plaques in their brain at 10 months old.

Effectively, one genetic abnormality cured the other.

Their cognition was also improved, although not fully.

Professor Yan said:

“Our study provides genetic evidence that preformed amyloid deposition can be completely reversed after sequential and increased deletion of BACE1 in the adult.

Our data show that BACE1 inhibitors have the potential to treat Alzheimer’s disease patients without unwanted toxicity.

Future studies should develop strategies to minimize the synaptic impairments arising from significant inhibition of BACE1 to achieve maximal and optimal benefits for Alzheimer’s patients.”

The study was published in the Journal of Experimental Medicine (Hu et al., 2018).

Could this discovery show the way to reversing dementia?

A build-up of toxic urea in the brain is a major cause of dementia, according to new research.

Toxic levels of urea have newly been linked to Huntington’s, a type of dementia.

Recent research has also linked urea to Alzheimer’s, the most common form of dementia.

Urea and ammonia — which are usually excreted in urine — can also build up in the brain, especially if the kidneys are unable to filter them out.

Drugs that are now commonly used to target urea could one day be used to help treat dementia.

Professor Garth Cooper, who led the study, said:

“This study on Huntington’s Disease is the final piece of the jigsaw which leads us to conclude that high brain urea plays a pivotal role in dementia.

Alzheimer’s and Huntington’s are at opposite ends of the dementia spectrum – so if this holds true for these types, then I believe it is highly likely it will hold true for all the major age-related dementias.

More research, however, is needed to discover the source of the elevated urea in HD, particularly concerning the potential involvement of ammonia and a systemic metabolic defect.

This could have profound implications for our fundamental understanding of the molecular basis of dementia, and its treatability, including the potential use of therapies already in use for disorders with systemic urea phenotypes.”

The study looked at brains donated by families for medical research along with genetically modified sheep.

Professor Cooper said:

“We already know Huntington’s Disease is an illness caused by a faulty gene in our DNA – but until now we didn’t understand how that causes brain damage – so we feel this is an important milestone.

Doctors already use medicines to tackle high levels of ammonia in other parts of the body Lactulose – a commonly used laxative, for example, traps ammonia in the gut.

So it is conceivable that one day, a commonly used drug may be able to stop dementia from progressing.

It might even be shown that treating this metabolic state in the brain may help in the regeneration of tissue, thus giving a tantalising hint that reversal of dementia may one day be possible.”

The study was published in the journal PNAS (Renee et al., 2017).

The sign comes 10 years before memory and thinking problems are obvious.

A worsening of anxiety symptoms could be an early sign of Alzheimer’s in older people, new research finds.

The symptom could help to diagnose the disease 10 years before problems with memory and thinking are obvious.

In this ‘preclinical’ phase, up to 10 years before disease onset, deposits of amyloid and tau proteins build up in the brain.

The study found that the greater these build-ups, the higher the symptoms of anxiety people experienced.

Dr Nancy Donovan, the study’s first author, explained:

“Rather than just looking at depression as a total score, we looked at specific symptoms such as anxiety.

When compared to other symptoms of depression such as sadness or loss of interest, anxiety symptoms increased over time in those with higher amyloid beta levels in the brain.

This suggests that anxiety symptoms could be a manifestation of Alzheimer’s disease prior to the onset of cognitive impairment.”

The conclusions come from a study of 270 people aged 62-90 years-old, who were followed over five years.

Their anxious-depressive symptoms predicted the build of amyloid plaques in the brain, which are, in turn, linked to the onset of Alzheimer’s disease.

Dr Donovan said:

“If further research substantiates anxiety as an early indicator, it would be important for not only identifying people early on with the disease, but also, treating it and potentially slowing or preventing the disease process early on.”

The study was published in the American Journal of Psychiatry (Donovan et al., 2018).

Alzheimer’s linked to condition that affects 1 in 5 people in the US.

Insomnia leads to a build up of the proteins linked to Alzheimer’s, new research finds.

Insomnia is thought to affect around 1 in 5 people in the US — somewhere between 50 and 70 million people.

In addition, around one-third of Americans do not get enough sleep.

A wakeful brain, though, produces more amyloid beta than the brain’s waste disposal system can cope with.

This could eventually lead to Alzheimer’s disease.

Professor Randall Bateman, who led the study, said:

“This study is the clearest demonstration in humans that sleep disruption leads to an increased risk of Alzheimer’s disease through an amyloid beta mechanism.

The study showed that it was due to overproduction of amyloid beta during sleep deprivation.”

The study looked at the effects of sleeping poorly on the brain in the short term.

Three groups were compared: some slept normally, some stayed up all night and others were given a sleeping aid.

Those who stayed up had amyloid beta levels some 25-30% higher.

This level is on a par with those genetically predisposed to Alzheimer’s.

Dr Brendan Lucey, the study’s first author, said:

“I don’t want anyone to think that they are going to get Alzheimer’s disease because they pulled an all-nighter in college.

One night probably has no effect on your overall risk of Alzheimer’s.

We are really much more concerned about people with chronic sleep problems.”

Amyloid beta is a normal byproduct of brain activity.

However, without adequate sleep, the brain cannot clear it away.

Dr Lucey said:

“Understanding how lack of sleep relates to the concentrations of amyloid beta in the brain will help direct future research into therapeutics.

This information could help us figure out how to reduce amyloid beta deposition over time in people whose sleep is chronically disrupted.”

Sleep medication may not provide much benefit, the study suggests.

Dr Lucey said:

“We were looking at healthy, well-rested adults.

This suggests that if you already are getting enough sleep, getting more sleep with the help of medication may not provide any benefit.”

The study was published in the journal Annals of Neurology (Lucey et al., 2017).

The cause of Alzheimer’s is not just in the brain.

Alzheimer’s disease could be a problem that involves the whole body, according to new research.

Alzheimer’s — the most common form of dementia — has usually been thought of as only a brain disease.

However, research now suggests the disease could be triggered elsewhere in the body.

Chinese research has shown that amyloid-beta — the protein thought central to Alzheimer’s — can contribute to the disease even when it comes from outside the brain.

The findings suggest drugs that might be able to target the kidney or liver to try and reduce toxic proteins before they reach the brain.

Professor Weihong Song, who led the research, said:

“The blood-brain barrier weakens as we age.

That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”

It is already known that the toxic amyloid-beta protein linked to Alzheimer’s is produced in the blood platelets, blood vessels and muscles.

Until now it was unclear whether it could pass into the brain.

Professor Song thinks the protein could be biochemically tagged to allow the liver or kidneys to clear it.

Professor Song added:

“Alzheimer’s disease is clearly a disease of the brain, but we need to pay attention to the whole body to understand where it comes from, and how to stop it.”

The study was published in the journal Molecular Psychiatry (Bu et al., 2017).

The best balance of fatty acids for brain health.

The right balance between omega-3 and omega-6 fatty acids may help promote healthy cognitive aging, new research finds.

While we are used to hearing about the benefits of the fatty acids in fish and fish oils, that is only half the story.

Omega-6 fatty acids can come from nuts, seeds and other oils.

Typically, Western diets have too much omega-6 and not enough omega-3.

Together, a balance of these fatty acids may help to reduce age-related decline and maintain the integrity of cortical structures.

Ms Marta Zamroziewicz, who led the research, said:

“We studied a primary network of the brain — the frontoparietal network — that plays an important role in fluid intelligence and also declines early, even in healthy aging.

In a separate study, we examined the white matter structure of the fornix, a group of nerve fibers at the center of the brain that is important for memory.”

The researchers examined the levels of polyunsaturated fatty acids in adults aged 65 to 75, along with their brain structure.

Ms Zamroziewicz explained that it takes more than just fish and fish oils to keep the brain healthy with age:

“A lot of research tells us that people need to be eating fish and fish oil to get neuroprotective effects from these particular fats, but this new finding suggests that even the fats that we get from nuts, seeds and oils can also make a difference in the brain.”

A second study found a link between a balanced amount of omega-3 and omega-6 fatty acids and greater memory preservation in older adults.

Ms Zamroziewicz explained:

“These findings have important implications for the Western diet, which tends to be misbalanced with high amounts of omega-6 fatty acids and low amounts of omega-3 fatty acids.”

Professor Aron Barbey, who co-authored the study, said:

“These two studies highlight the importance of investigating the effects of groups of nutrients together, rather than focusing on one at a time.

They suggest that different patterns of polyunsaturated fats promote specific aspects of cognition by strengthening the underlying neural circuits that are vulnerable to disease and age-related decline.”

The study was published in the journal Nutritional Neuroscience (Zamroziewicz et al., 2017).

Dementia risk reduced in 10 1-hour sessions — benefits seen 10 years later.

A type of mental exercise has been linked for the first time to a reduced risk of dementia.

The training is called ‘speed processing’ and involves identifying objects and their location on a screen.

As people improve at this cognitive task, the software speeds up.

The speed training was effective where more traditional memory and reasoning training had little effect on dementia.

Professor Frederick W. Unverzagt, who led the study, said it was comparatively easy training:

“We would consider this a relatively small dose of training, a low intensity intervention.

The persistence — the durability of the effect was impressive.”

The initial training was carried out in 10 one-hour sessions.

Most people subsequently did an extra four booster sessions.

Compared with a control group, and other comparisons, the speed processing training reduced dementia risk by 29%.

People were followed up one, two, three, five and 10 years later.

Impressively, the effects of the training were still there after 10 years.

This is some of the first strong evidence that mental training can help fight dementia.

The study was published in the journal Alzheimer’s & Dementia: Translational Research & Clinical Interventions (Edwards et al., 2017).

During slow-wave or deep sleep, the brain is cleared of waste products.

A single night of disrupted sleep is enough to increase a brain protein linked to Alzheimer’s, new research shows.

A full week of poor sleep causes increases in another brain protein that is also linked to Alzheimer’s.

The findings may help to explain why poor sleep has been linked to Alzheimer’s.

Professor David M. Holtzman, who led the study, said:

“We showed that poor sleep is associated with higher levels of two Alzheimer’s-associated proteins.

We think that perhaps chronic poor sleep during middle age may increase the risk of Alzheimer’s later in life.”

Alzheimer’s disease is characterised by gradual cognitive decline and memory loss.

Previous research has shown a link between poor sleep and cognitive problems.

For example, people with sleep apnea — when breathing stops repeatedly during the night — are at risk of developing mild cognitive impairment ten years earlier.

For the study, the effects of sleep apnea were simulated.

People’s deep sleep was disrupted in such a way that they did not wake during the night, but they also did not feel refreshed in the morning.

Levels of the two proteins — called amyloid beta and tau — were both measured by spinal taps.

Dr Yo-El Ju, the study’s first author, explained the results:

“We were not surprised to find that tau levels didn’t budge after just one night of disrupted sleep while amyloid levels did, because amyloid levels normally change more quickly than tau levels.

But we could see, when the participants had several bad nights in a row at home, that their tau levels had risen.”

The scientists do not think that one night or a week of poor sleep is enough to cause Alzheimer’s.

The protein levels probably return to normal with better sleep.

Dr Ju said:

“The main concern is people who have chronic sleep problems.

I think that may lead to chronically elevated amyloid levels, which animal studies have shown lead to increased risk of amyloid plaques and Alzheimer’s.”

It is vital that we get enough slow-wave or deep sleep, as this is when the brain is cleared of waste products.

Dr Ju said:

“Many, many Americans are chronically sleep-deprived, and it negatively affects their health in many ways.

At this point, we can’t say whether improving sleep will reduce your risk of developing Alzheimer’s.

All we can really say is that bad sleep increases levels of some proteins that are associated with Alzheimer’s disease.

But a good night’s sleep is something you want to be striving for anyway.”

The study was published in the journal Brain (Ju et al., 2017).

Scientists have slowed down the cognitive and physical ageing process in mice.

Brain cells in the hypothalamus govern how fast the mind and body ages, new research finds.

The hypothalamus is a part of the brain important in how we grow, develop, reproduce and how our metabolism works.

In the hypothalamus there are a small number of cells that control our ageing.

Professor Dongsheng Cai, who led the study, said:

“Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging.

But we also found that the effects of this loss are not irreversible.

By replenishing these stem cells or the molecules they produce, it’s possible to slow and even reverse various aspects of aging throughout the body.”

The scientists tried disrupting these brain cells in mice to test the effect.

Professor Cai explained the results:

“This disruption greatly accelerated aging compared with control mice, and those animals with disrupted stem cells died earlier than normal.”

Next, the researchers tried injecting stem cells into this area of the brains of mice who were middle-aged or old.

The effect was to slow or prevent ageing.

The mice were better preserved both mentally and physically after being given the stem cells.

The finding could lead to therapies for extending the human lifespan and improving cognition in advanced years.

The study was published in the journal Nature (Zhang et al., 2017).

Brain illustration image from Shutterstock