Category: Dementia

Michael J Fox, who suffers from Parkinson’s, is an advocate for research into the disease.

Drugs currently used to treat malaria could also provide a treatment for Parkinson’s disease, a new study reports.

Parkinson’s disease is caused by a loss of cells in part of the brain called the substantia nigra.

This leads to a reduction in the production of a neurotransmitter called dopamine.

Since dopamine helps regulate movement, Parkinson’s causes tremors and involuntary movements, as well as stiff and inflexible muscles, among other symptoms.

The new research, carried out by researchers in the US and Singapore, could be a breakthrough.

Dr Yoon Ho Sup, one of the study’s authors, said:

“Our discovery brings hope for the millions of people suffering from Parkinson’s disease, as the drugs that we have found to have worked in the laboratory tests have already been used to treat malaria in patients for decades.

Our research also shows that existing drugs can be repurposed to treat other diseases and once several potential drugs are found, we can redesign them to be more effective in combating their targeted diseases while reducing the side effects.”

The two anti-malaria drugs, Chloroquine and Amodiaquine, were among around 1,000 tested.

Rats with Parkinson’s showed improvements in their behaviour and no signs of the disease after being treated with the drug.

Professor Kwang-Soo Kim, another of the study’s authors, and expert on Parkinsons’, explained some of the problems with existing treatments:

“…[existing] pharmacological and surgical treatments address the patient’s symptoms, such as to improve mobility functions in the early stages of the disease, but the treatments cannot slow down or stop the disease process.

Backed by various lines of scientific evidence, Nurr1 is known to be a potential drug target to treat Parkinson’s.

Despite great efforts from pharmaceutical companies and academia, no one has managed to find a molecule which can directly bind to it and activate it, except for us.”

It is hoped these drugs can be modified to provide a better treatment for Parkinson’s than those that already exist.

The study was published in the Proceedings of the National Academy of Sciences (Kim et al., 2015).

Michael J Fox image from Shutterstock 

Tests predict ten-fold increase in Alzheimer’s risk 18 years in advance.

Low scores on memory and thinking tests could signal Alzheimer’s 18 years in advance, a new study finds.

Dr Kumar B. Rajan, the study’s lead author, said:

“The changes in thinking and memory that precede obvious symptoms of Alzheimer’s disease begin decades before.

While we cannot currently detect such changes in individuals at risk, we were able to observe them among a group of individuals who eventually developed dementia due to Alzheimer’s.”

In the study, over two thousand people from Chicago were given tests of memory and thinking every three years over 18 years.

Around one in five of the participants, whose average age was 73, developed the disease during the study.

Lower scores on the tests predicted a ten-fold increase in the risk of developing the disease.

Relatively small decreases in performance on the test were linked to large increases in Alzheimer’s risk.

Dr Rajan said:

“A general current concept is that in development of Alzheimer’s disease, certain physical and biologic changes precede memory and thinking impairment.

If this is so, then these underlying processes may have a very long duration.

Efforts to successfully prevent the disease may well require a better understanding of these processes near middle age.”

The study was published in the journal Neurology (Rajan et al., 2015).

Alzheimer’s photo from Shutterstock

How Alzheimer’s could be linked to sleep quality.

Poor sleep is a channel through which Alzheimer’s disease can be triggered, a new study finds.

Professor Matthew Walker, one of the neuroscientist who authored the study, said:

“This discovery offers hope.

Sleep could be a novel therapeutic target for fighting back against memory impairment in older adults and even those with dementia.”

The study is one of the first to look at human rather than animal subjects in this way.

Professor William Jagust, a leading expert on Alzheimer’s disease who co-led the study, said:

“Over the past few years, the links between sleep, beta-amyloid, memory, and Alzheimer’s disease have been growing stronger.

Our study shows that this beta-amyloid deposition may lead to a vicious cycle in which sleep is further disturbed and memory impaired.”

For the research, 26 older people without dementia were given memory tests and had their brains scanned before and after sleep.

Professor Walker explained:

“The more you remember following a good night of sleep, the less you depend on the hippocampus and the more you use the cortex.

It’s the equivalent of retrieving files from the safe storage site of your computer’s hard drive, rather than the temporary storage of a USB stick.

The more beta-amyloid you have in certain parts of your brain, the less deep sleep you get and, consequently, the worse your memory.

Additionally, the less deep sleep you have, the less effective you are at clearing out this bad protein.

It’s a vicious cycle.

But we don’t yet know which of these two factors — the bad sleep or the bad protein — initially begins this cycle. Which one is the finger that flicks the first domino, triggering the cascade?”

Dr Bryce Mander, study’s lead author, said:

“The data we’ve collected are very suggestive that there’s a causal link.

If we intervene to improve sleep, perhaps we can break that causal chain.”

This ties in with evidence of how sleep fights toxins in the brain.

Professor Walker said:

“Sleep is helping wash away toxic proteins at night, preventing them from building up and from potentially destroying brain cells,.

It’s providing a power cleanse for the brain.

The study was published in the journal Nature Neuroscience (Walker et al., 2015).

Alzheimer’s photo from Shutterstock

How to reduce the risk of dementia, what causes it and a potential miracle cure.

Here are eight fascinating new studies on dementia and it’s most common form, Alzheimer’s disease.

Below you can find out what causes dementia, how the risk can be reduced and the latest technologies being used in the fight against it.

(Click the links for longer descriptions of the studies.)

How to reduce the risk

Some of the factors linked to a reduced risk of developing Alzheimer’s are well-known.

Eating the right diet, doing some exercise, getting checked out by a doctor and also giving the brain a workout, are all likely to be effective.

A recent study found impressive cognitive gains for people doing all four.

For specific activities linked to a lower risk, why not try computer use, as well as socialising and doing arts and crafts.

A new study has found that doing these in middle age may help preserve memory in later years.

Obesity on its own, though, does not seem to be linked to dementia — indeed, it may even reduce the risk.

Surprisingly, four very common medicines have also been linked to dementia risk.

They are:

1. Doxepin (Sinequan) – an older antidepressant.
2. Chlorpheniramine (Chlor-Trimeton) – an antihistamine used to treat hayfever.
3. Diphenhydramine (Benadryl) – another antihistamine often used to treat hayfever and sometimes used to aid sleep.
4. Oxybutynin (Ditropan) – for bladder control.

The MIND diet

For more specific advice about what to eat and what to avoid, check out the recent ‘MIND diet’ study.

The diet could reduce the risk of developing Alzheimer’s by over 50%.

Along with many of the usual suspects, the researchers identified one specific food which is particularly potent for protecting the brain: blueberries.

Another key ingredient, according to nutritional epidemiologists, is vitamin K, which is contained in leafy vegetables.

Older adults in the study who ate just two servings of leafy vegetables each day kept their brains around eleven years younger.

The real cause of Alzheimer’s?

There has been a lot of scientific debate just recently about what causes Alzheimer’s.

One recent study claimed that amyloid, a toxic protein frequently linked to Alzheimer’s may not be the main driver of the disease after all.

The ‘real’ cause of Alzheimer’s is a dysfunctional ‘tau’ protein, the scientists claimed.

If this turns out to be true, that will mean a lot of scientific work has been in vain.

But, hey, that’s science for you — research can go down loads of blind alleys before it finds a way through.

A miracle cure?

My award for best recent miracle cure goes to Australian scientists who have found a potential Alzheimer’s treatment that can restore memory using ultrasound technology.

The technique — which has been successfully tested on mice — does not involve drugs, but high frequency sound waves.

Professor Jürgen Götz, the director of the Clem Jones Centre for Ageing Dementia Research in Australia, and one of the study’s authors, said:

“We’re extremely excited by this innovation of treating Alzheimer’s without using drug therapeutics.

The ultrasound waves oscillate tremendously quickly, activating microglial cells that digest and remove the amyloid plaques that destroy brain synapses.”

Given that some scientists are questioning if amyloid is the real culprit, this miracle cure might not be so hot after all.

Runner-up in the miracle cure category goes to the life-extending protein called ‘klotho’.

A mouse study has found it may increase learning and memory and ward off Alzheimer’s.

Dr Dena Dubal, who led the study, said:

“It’s remarkable that we can improve cognition in a diseased brain despite the fact that it’s riddled with toxins.

In addition to making healthy mice smarter, we can make the brain resistant to Alzheimer-related toxicity.

Without having to target the complex disease itself, we can provide greater resilience and boost brain functions.”

Alzheimer’s photo from Shutterstock

New research links living near these to a 46% increase in stroke risk.

Living further away from major roadways has been linked to better brain health by new research.

Long-term exposure to even moderate levels of air pollution, the study found, is bad for the brain.

Air pollution may cause poor cognitive function and ‘silent strokes’, which have been linked to dementia.

The study also found that people exposed to more air pollution had smaller brains.

Dr Elissa Wilker, an epidemiologist at Beth Israel Deaconess Medical Center who led the study, said:

“This is one of the first studies to look at the relationship between ambient air pollution and brain structure.

Our findings suggest that air pollution is associated with insidious effects on structural brain aging, even in dementia- and stroke-free individuals.”

The study looked at how far people lived from the nearest roadway.

It also used satellite imagery to work out their average exposure to fine particulate matter.

All the participants in the study were over 60 and free from dementia and stroke.

Professor Sudha Seshadri, a neurologist at Boston University School of Medicine and one of the study’s authors, explained the results:

“This study shows that for a 2 microgram per cubic meter of air (μg/m3) increase in PM2.5 [particular matter bigger than 2.5 millionths of a meter], a range commonly observed across major US cities, on average participants who lived in more polluted areas had the brain volume of someone a year older than participants who lived in less polluted areas.

They also had a 46 percent higher risk of silent strokes on MRI.

This is concerning since we know that silent strokes increase the risk of overt strokes and of developing dementia, walking problems and depression.

We now plan to look at more the impact of air pollution over a longer period, its effect on more sensitive MRI measures, on brain shrinkage over time, and other risks including of stroke and dementia.”

Particles of pollution can travel deep into the lungs and have been linked to strokes, heart attacks and other cardiovascular problems.

Dr Elissa Wilker said:

“These results are an important step in helping us learn what is going on in the brain.

The mechanisms through which air pollution may affect brain aging remain unclear, but systemic inflammation resulting from the deposit of fine particles in the lungs is likely important.”

The study was published in the journal Stroke (Wilker et al., 2015).

Tree brain image from Shutterstock

New study suggests scientists have been looking in the wrong place for the cause of Alzheimer’s disease.

Alzheimer’s disease may be caused by immune cells that start to behave abnormally, a new study finds.

Scientists have also used a drug to block this process and slow the disease in mice.

The immune cells, instead of protecting the body, consume an important nutrient called arginine.

Professor Carol Colton, who led the study, said:

“If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease.”

Matthew Kan, the study’s first author, said the research came from a totally new direction:

“It’s surprising, because [suppression of the immune system is] not what the field has been thinking is happening in AD.

Instead, scientists have previously assumed that the brain releases molecules involved in ramping up the immune system, that supposedly damage the brain.”

The scientist found that immune cells called microglia may be at the heart of Alzheimer’s.

When they studied the disease process in mice, it was these microglia — part of the immune system — that seemed to be causing the disease.

When the researchers blocked the reduction of the amino acid arginine, mice performed better on memory tests and had fewer tangles and plaques in their brains that are characteristic of Alzheimer’s disease.

Mr Kan said:

“All of this suggests to us that if you can block this local process of amino acid deprivation, then you can protect — the mouse, at least — from Alzheimer’s disease.”

None of this means that people should consider supplementing their diet with arginine.

It is difficult for arginine to cross the blood-brain barrier and in any case would be broken down by the disease process.

Professor Colton said:

“We see this study opening the doors to thinking about Alzheimer’s in a completely different way, to break the stalemate of ideas in AD.

The field has been driven by amyloid for the past 15, 20 years and we have to look at other things because we still do not understand the mechanism of disease or how to develop effective therapeutics.”

The study was published in the Journal of Neuroscience (Kan et al., 2015).

Alzheimer’s photo from Shutterstock

New study finds a surprising link between body weight and dementia risk.

Underweight people are one-third more likely to develop dementia than those of a healthy weight, a new study finds.

It also found that very obese people are 30% less likely to develop dementia than those with a healthy weight.

This surprising conclusion comes from the largest ever study of middle-aged people’s dementia risk and body weight.

The findings fly in the face of previous research suggesting a positive connection between obesity and dementia.

Professor Stuart Pocock, from the London School of Hygiene & Tropical Medicine, who led the study, said:

“Our results suggest that doctors, public health scientists, and policy makers need to re-think how to best identify who is at high risk of dementia.

We also need to pay attention to the causes and public health consequences of the link between underweight and increased dementia risk which our research has established.

However, our results also open up an intriguing new avenue in the search for protective factors for dementia — if we can understand why people with a high BMI have a reduced risk of dementia, it’s possible that further down the line, researchers might be able to use these insights to develop new treatments for dementia.”

For the research data was analysed from nearly two million people.

They were followed up over almost a decade to check their weight and any dementia diagnosis.

The results showed that very obese people (those with a BMI over 40) were 29% less likely to develop dementia than those of a normal, healthy weight.

Below a healthy weight (a BMI of 25), the dementia risk increased.

Above a healthy weight, though, the dementia risk continued to decrease, but more slowly.

Dr Nawab Qizilbash, the study’s first author, said:

“The reasons why a high BMI might be associated with a reduced risk of dementia aren’t clear, and further work is needed to understand why this might be the case.

If increased weight in mid-life is protective against dementia, the reasons for this inverse association are unclear at present.

Many different issues related to diet, exercise, frailty, genetic factors, and weight change could play a part.”

The research was published in The Lancet Diabetes & Endocrinology journal (Qizilbash et al., 2015)

Tree head image from Shutterstock

New dementia treatment can also reduce depression and anxiety.

Scientists have found that sending electrical impulses into the brain can help new brain cells to grow.

The technique could be used as a dementia treatment as well as for brain injuries.

Deep brain stimulation, as it is known, is already used for certain neurological conditions, like Dystonia and tremors.

Scientists have found that stimulating the front of the brain with small amounts of electricity can help new neurons grow.

Professor Ajai Vyas, one of the study’s authors, said:

“The findings from the research clearly show the potential of enhancing the growth of brain cells using deep brain stimulation.

Around 60 per cent of patients do not respond to regular anti-depressant treatments and our research opens new doors for more effective treatment options.”

Dr Lim Lee Wei, another of the study’s authors, said:

“No negative effects have been reported in such prefrontal cortex stimulation in humans and studies have shown that stimulation also produces anti-depression effects and reduces anxiety.

Memory loss in older people is not only a serious and widespread problem, but signifies a key symptom of dementia.

At least one in 10 people aged 60 and above in Singapore suffer from dementia and this breakthrough could pave the way towards improved treatments for patients.”

The study was carried out on middle-aged rats that had electrodes implanted into their brains.

These sent out small electrical impulses.

Scientists found that new brain cells were formed in the hippocampus, an area which is vital for memory in rats and humans.

Tests on the rats showed their memory had been improved.

Professor Ajai continued:

“Extensive studies have shown that rats’ brains and memory systems are very similar to humans.

The electrodes are harmless to the rats, as they go on to live normally and fulfil their regular (adult) lifespan of around 22 months.”

The research was published in the journal eLife (Liu et al., 2015)

Brain grow image from Shutterstock

Amyloid proteins may not be the cause of Alzheimer’s after all.

The real cause of Alzheimer’s is a dysfunctional ‘tau’ protein, a new study of over 3,600 brains finds.

Amyloid, a toxic protein frequently linked to Alzheimer’s may not be the main driver of the disease after all.

The tau protein normally helps stabilise the brain’s structure.

The fight against Alzheimer’s should be focused on the tau protein from now on, the researchers think.

Dr Melissa Murray, a neuroscientist at the Mayo Clinic in Jacksonville, and one of the study’s authors, said:

“The majority of the Alzheimer’s research field has really focused on amyloid over the last 25 years.

Initially, patients who were discovered to have mutations or changes in the amyloid gene were found to have severe Alzheimer’s pathology — particularly in increased levels of amyloid.

Brain scans performed over the last decade revealed that amyloid accumulated as people progressed, so most Alzheimer’s models were based on amyloid toxicity.

In this way, the Alzheimer’s field became myopic.”

The research looked at 3,618 brains stored in the Mayo Clinic.

1,375 had confirmed Alzheimer’s and had died at different ages, providing a timeline of the disease’s progression.

Dr. Murray explained:

“Imagine looking at the rings of a tree — you can identify patterns, like the changing seasons and the aging of the tree, when viewing the tree’s cross-section.

Studying brains at different stages of Alzheimer’s gives us a perspective of the cognitive impact of a wide range of both amyloid and tau severity, and we were very fortunate to have the resource of the Mayo brain bank, in which thousands of people donated their postmortem brains, that have allowed us to understand the changes in tau and amyloid that occur over time.”

The researchers found that it was the tau protein, not amyloid, that predicted the onset of cognitive decline.

Dr. Murray explained the importance of the tau protein:

“Tau can be compared to railroad ties that stabilize a train track that brain cells use to transport food, messages and other vital cargo throughout neurons.

In Alzheimer’s, changes in the tau protein cause the tracks to become unstable in neurons of the hippocampus, the center of memory.

The abnormal tau builds up in neurons, which eventually leads to the death of these neurons.

Evidence suggests that abnormal tau then spreads from cell to cell, disseminating pathological tau in the brain’s cortex.

The cortex is the outer part of the brain that is involved in higher levels of thinking, planning, behavior and attention — mirroring later behavioral changes in Alzheimer’s patients.

Amyloid, on the other hand, starts accumulating in the outer parts of the cortex and then spreads down to the hippocampus and eventually to other areas.

Our study shows that the accumulation of amyloid has a strong relationship with a decline in cognition.

When you account for the severity of tau pathology, however, the relationship between amyloid and cognition disappears — which indicates tau is the driver of Alzheimer’s,”

The study is published in the journal Brain (Murray et al., 2015).

Alzheimer’s photo from Shutterstock

Although it’s in almost every fridge, few Americans have enough of this healthy brain food.

Milk consumption has been linked to higher levels of naturally-occurring antioxidants in the brain, a new study finds.

Despite this, few Americans reach the recommended daily intake for this healthy brain food.

Professor Debra Sullivan, chair of dietetics at University of Kansas Medical Center and one of the study’s authors, said:

“We have long thought of milk as being very important for your bones and very important for your muscles.

This study suggests that it could be important for your brain as well.”

The study of healthy older adults found that glutathione levels were higher in those drinking more milk.

Glutathione may help to stave off the effects of oxidative stress on the brain.

Professor Sullivan explained the importance of oxidative stress:

“You can basically think of this damage like the build-up of rust on your car.

If left alone for a long time, the buildup increases and it can cause damaging effects.”

Oxidative stress is thought to be involved in the development of Alzheimer’s and Parkinson’s disease along with many other conditions.

Dr In-Young Choi, the study’s first author, said:

“Antioxidants are a built-in defense system for our body to fight against this damage, and the levels of antioxidants in our brain can be regulated by various factors such as diseases and lifestyle choices.”

Healthy brain food

The study of the healthy brain food involved 60 older individuals.

Their diets were tracked in the days before having a brain scan.

Dr Choi explained that they used the latest technology to examine participants’ brains:

“Our equipment enables us to understand complex processes occurring that are related to health and disease.

The advanced magnetic resonance technology allowed us to be in a unique position to get the best pictures of what was going on in the brain.”

Few Americans reach three servings of dairy a day, which is the recommended intake.

However, the study showed that the more dairy people had had recently, the higher the levels of the antioxidant.

Dr Choi said:

“If we can find a way to fight this by instituting lifestyle changes including diet and exercise, it could have major implications for brain health.”

The study is published in The American Journal of Clinical Nutrition (Choi et al., 2015).

Woman and fridge image from Shutterstock