Category: Dementia

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)

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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

These simple lifestyle changes improve reasoning, problem-solving, processing speed and may ultimately prevent dementia.

Healthy eating, brain training, exercise and good medical management may prevent dementia, a new study suggests.

The Finnish study is the first ever to properly test a special programme to prevent age-related cognitive decline.

The two-year study had 1,260 people aged 60-77 randomly assigned to either receive some general health advice or the special programme.

Here is some of the advice those in the special programme group were given:

1. Diet

People were advised to eat plenty of fruit and vegetables, wholegrain cereals and low-fat milk and meat products.

They were also told to eat no more than 50g of sugar each day and to have at least two portions of fish each week.

2. Cognitive training

People were given computer brain training sessions and given advice on memory and reasoning strategies they could use.

This could probably be substituted with generally keeping mentally active.

This might include things like reading, doing puzzles and being engaged with life.

3. Exercise

For physical exercise, the advice was to do some strength training, one to three times a week.

Aerobic exercise was recommended two to five times a week.

The exercise advice was tailored to the individual: some were able to do more, others less.

4. Medical management

Blood pressure was checked, along with weight and BMI.

Based on this they were given more recommendations for potential lifestyle changes.

Participants were advised to see their doctor for any medication they might need.

Prevent dementia?

The study found that after two years, those who had received the special programme scored 25% higher on a neuropsychological test.

On a test of processing speed, though, the special programme group did 150% better.

On a measure of executive functioning — which controls memory, reasoning and problem solving — the special programme group had scores 83% higher.

Professor Miia Kivipelto, who led the research, said:

“Much previous research has shown that there are links between cognitive decline in older people and factors such as diet, heart health, and fitness.

However, our study is the first large randomised controlled trial to show that an intensive program aimed at addressing these risk factors might be able to prevent cognitive decline in elderly people who are at risk of dementia.”

The study now continues for at least another seven years to look at whether it can prevent dementia and Alzheimer’s diagnoses.

The study was published in The Lancet (Ngandu et al., 2015).

Time for change image from Shutterstock

The young age at which amyloid protein, a hallmark of Alzheimer’s, begins to appear in the brain.

Amyloid protein, which is a hallmark of Alzheimer’s disease, has been detected in people as young as 20, a new study finds.

This is much earlier than any scientists previously thought.

Amyloid protein is strongly associated with Alzheimer’s disease.

It eventually forms in clumps outside the neurons.

Professor Changiz Geula, who led the study, said:

“Discovering that amyloid begins to accumulate so early in life is unprecedented.

This is very significant.

We know that amyloid, when present for long periods of time, is bad for you.”

Alzheimer’s study

The research looked at the brains of deceased people from ages 20 to 95.

Some had died young with no signs of dementia, while others had died later with or without Alzheimer’s.

The researchers focused on an area in the basal forebrain which is critical to memory and attention.

These neurons are the first to die in both normal ageing and in Alzheimer’s.

They found that the amyloid proteins began accumulating inside these neurons from as early as 20-years-old.

Together these proteins can form toxic lumps in the brain.

Older individuals and those with Alzheimer’s had larger toxic lumps of amyloid.

Professor Geula said:

“This points to why these neurons die early.

The small clumps of amyloid may be a key reason.

The lifelong accumulation of amyloid in these neurons likely contributes to the vulnerability of these cells to pathology in aging and loss in Alzheimer’s.”

The clumps damage the brain by killing neurons and by secreting more amyloid outside the cell.

Professor Geula said:

“It’s also possible that the clumps get so large, the degradation machinery in the cell can’t get rid of them, and they clog it up.”

The research is published in the journal Brain (Baker-Nigh et al., 2015)

MRI image from Shutterstock

Potential new treatment for Alzheimer’s and other cognitive disorders.

A life-extending protein called ‘klotho’ can increase learning and memory and ward off Alzheimer’s a new study reports.

Scientists at the University of California and the Gladstone Institutes have found that increasing the levels of klotho boosted learning and cognition in mice with Alzheimer’s toxins in their brains.

Klotho is an enzyme that naturally occurs in humans which is thought to be involved in the ageing process.

It takes its name from the entity in Greek mythology called ‘Clotho’, who was one of the ‘fates’ who were supposed to control the thread of people’s lives.

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.”

For the research, published in The Journal of Neuroscience, neuroscientists bred mice which had Alzheimer’s disease, but also had high levels of the klotho protein throughout their bodies (Dubal et al., 2015).

Normally mice with Alzheimer’s die earlier, have cognitive problems and abnormal brain activity, just like humans with the disease.

These mice, though, behaved normally and did not die prematurely.

Apparently the Klotho protein counteracted the effects of the Alzheimer’s disease.

Scientists are not yet sure why the klotho protein has these effects.

One theory is that klotho affects a neurotransmitter receptor in the brain called NMDA, which is crucial to learning and memory.

Professor Lennart Mucke, one of the study’s authors, said:

“We are encouraged in this regard by the strong similarities we found between klotho’s effects in humans and mice in our earlier study.

We think this provides good support for pursuing klotho as a potential drug target to treat cognitive disorders in humans, including Alzheimer’s disease.”

• See also: Longevity Gene May Enhance Cognition

MRI scan image from Shutterstock