Blueberries may help combat dementia and alzheimers

Snacking on blueberries from middle age could prevent dementia developing decades later, scientists say.

Experts told a major US conference that a compound in the berries may strengthen the brain’s defences against Alzheimer’s.

In the absence of effective drugs, a nutritional option ‘represents a potentially potent approach to mitigate risk for late-life dementia’, they said.

Alzheimer’s and other forms of dementia affect some 850,000 Britons and cost the economy £26billion a year.

With the search for new medicines largely fruitless, despite hundreds of drug trials and billions of pounds of funding, some experts believe more emphasis should be placed on the benefits of a healthy diet.

Candidates include the humble blueberry, a ‘superfood’ already credited with lowering the risk of heart disease and cancer.

University of Cincinnati researcher Robert Krikorian (CORR) studied 47 men and women aged 68-plus who had been diagnosed with mild cognitive impairment.

The term covers the slight memory lapses that often, although not always, develop into full-blown dementia.

All were given a placebo powder or one made of freeze-dried blueberries to take once a day for four months.

The blueberry powder been specially made for the study, and one sachet contained the equivalent of a small teacupful of berries.

The volunteers were also put through a battery of mental tests at the study’s start and end, with a focus on memory and thinking skills that are eroded by dementia.

The results showed that the berries seemed to give the ageing brain a boost.

Dr Krikorian said: ‘There was a significant improvement in cognitive function in those who had the blueberry powder, compared with those who took the placebo.’

In addition scans showed the brain was more active in those who had taken the blueberry powder.

The researcher believes the benefits are due to anthocyanins, the plant chemicals that give the berries their deep blue/purple colour.

Blueberries
Blueberries

They are thought to act on the brain in various ways, including boosting blood flow, cutting inflammation, and enhancing the passage of information between cells.

The chemicals may also boost cells’ defences, an American Chemical Society conference heard.

In a second study of people who hadn’t been diagnosed with any memory problems, but simply felt they were becoming more forgetful, the berries also helped boost cognition, although to a lesser extent.




When previous research is factored in, Dr Krikorian, who received funding from the US government, as well as from berry growers, says all the evidence points to blueberries having the potential to prevent the onset of dementia.

He said: ‘Our findings corroborate those of previous animal studies and preliminary human studies, adding further support to the notion that blueberries can have a real benefit in improving memory and cognitive function in older adults.’

He now wants to study people in their 50s and early 60s whose weight, blood pressure or other medical condition puts them at higher than usual risk of Alzheimer’s.

But, in the meantime, he advises healthy adults to stock up on blueberries.

And with research suggesting Alzheimer’s may eat away at the brain for decades before symptoms start to show, he says it is important to protect the brain from middle-age.

Dr Krikorian said: ‘I believe that berry supplementation and, in particular, blueberry supplementation, may reduce the risk for late-life cognitive decline.

‘The minimum dose is not clear but data suggest that taking blueberries several times a week should be beneficial.’

Brain’s immune response may hold cure to dementia

Alzheimer’s could be prevented and even cured by boosting the brain’s own immune response, scientists at Stanford University believe.

Researchers discovered that nerve cells die because cells which are supposed to clear the brain of bacteria, viruses and dangerous deposits, stop working.

These cells, called ‘microglia’ function well when people are young, but when they age, a single protein called EP2 stops them operating efficiently.

Now scientists have shown that blocking the protein allows the microglia to function normally again so they can hoover up the dangerous sticky amyloid-beta plaques which damage nerve cells in Alzheimer’s disease.

The researchers found that, in mice, blocking EP2 with a drug reversed memory loss and myriad other Alzheimer’s-like features in the animals.

“Microglia are the brain’s beat cops,” said Dr Katrin Andreasson, Professor of neurology and neurological sciences at Stanford University School of Medicine.

“Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology.”

By 2015 there will be 850,000 people with dementia in the UK, with Alzheimer’s disease being the most common type. The disease kills at least 60,000 people each year.

Microglial cells make up around 10 to 15 per cent of cells in the brain. They act as a frontline defence, looking for suspicious activities and materials. When they spot trouble, they release substances that recruit other microglia to the scene which then destroy and get rid of any foreign invaders.

Alzheimer's
Alzheimer’s

They also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells including clusters of amyloid-beta which aggregate as gummy deposits and break the connections between neurons, causing loss of memory and spatial awareness. These clusters are believed to play a substantial role in causing Alzheimer’s.

“The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation,” added Dr Andreasson. “If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation.”


The scientists discovered that in young mice, the microglia kept the sticky plaques under control. But when experiments were done on older mice, the protein EP2 swung into action and stopped the microglia producing enzymes which digested the plaques.

Similarly mice which were genetically engineered not to have EP2 did not develop Alzheimer’s disease, even when injected with a solution of amyloid-beta, suggesting that their cells were getting rid of the protein naturally.

And for those mice who developed Alzheimer’s, blocking EP2 reversed memory decline.

Now Stanford is hoping to produce a compound which only blocks EP2 to prevent unnecessary side effects.

The study was published in the Journal of Clinical Investigation.