Category: Dementia

The brain is particularly sensitive during the middle years.

The brains of obese individuals are physiologically 10 years older than lean individuals, new research finds.

Scientists looked at the brain’s white matter.

The white matter is the tissue that connects the areas and enables them to communicate with each other.

(In the images above, the white matter, confusingly, is in yellow, and it shows one subject with a BMI of 19.5 on the left and another with a BMI of 43.4 on the right.)

Dr Lisa Ronan, first author of this study, said:

“As our brains age, they naturally shrink in size, but it isn’t clear why people who are overweight have a greater reduction in the amount of white matter.

We can only speculate on whether obesity might in some way cause these changes or whether obesity is a consequence of brain changes.”

The study looked at the brains of 473 people aged between 20 and 87.

Overweight individuals had significantly less white matter in their brains than lean individuals.

The differences were only seen from middle-age onwards.

Professor Paul Fletcher, senior author of the study, added:

“We’re living in an ageing population, with increasing levels of obesity, so it’s essential that we establish how these two factors might interact, since the consequences for health are potentially serious.

The fact that we only saw these differences from middle-age onwards raises the possibility that we may be particularly vulnerable at this age.

It will also be important to find out whether these changes could be reversible with weight loss, which may well be the case.”

Professor Sadaf Farooqi, co-author of the study, said:

“We don’t yet know the implications of these changes in brain structure.

Clearly, this must be a starting point for us to explore in more depth the effects of weight, diet and exercise on the brain and memory.”

Despite the differences in brain volume, there were no deficits in cognitive abilities in overweight or obese people.

The study was published in the journal Neurobiology of Aging (Ronan et al., 2016).

Image credit: Dr Lisa Ronan

Until now brain training has proved more of a fad than a useful a treatment.

Computer-based brain training can halve the incidence of dementia, a surprising new study finds.

So far brain training has proved more of a fad than a useful a treatment.

But now research carried out over 10 years has found that a relatively small amount of brain training reduced older people’s chances of developing dementia dramatically.

For the study, healthy older adults did 10 brain training sessions of just over an hour.

They then had four further booster sessions a few years later.

Among the 2,832 people who started the study, 14% in the control group had developed dementia 10 years later.

This figure for those who had received the brain training was just 8.2%.

In general psychologists and others have found that brain training only produces relatively modest or inconsequential benefits.

So this study comes as a surprise.

Dr Jerri Edwards, the study’s first author, said:

“We believe this is the first time a cognitive training intervention has been shown to protect against cognitive impairment or dementia in a large, randomized, controlled trial.

Next, we’d like to get a better grasp on what exactly is the right amount of cognitive training to get the optimal benefits.”

The results could be down to the type of training that people were doing.

The training in this study encouraged them to speed up their processing.

Speed-of-processing training may be the key to the protective effect against dementia.

Alternatively, it may be that the brain training encouraged people to change their life in some way.

Some participants reported that the brain training had inspired them to keep intellectually engaged.

Dr Maria Carrillo, one of the study’s authors, said:

“The Alzheimer’s Association believes there is sufficiently strong evidence to conclude that lifelong learning and certain types of cognitive training may reduce the risk of cognitive decline.

These new 10-year findings are evidence that it may hold true for dementia as well as cognitive decline.”

The study was presented at the Alzheimer’s Association International Conference 2016 in Toronto.

Thinking image from Shutterstock

Vaccine could be used to immunise healthy people or treat these already suffering.

A newly developed vaccine against Alzheimer’s disease could be ready in 3 to 5 years, scientists claim.

Alzheimer’s disease is newly diagnosed in around 48 million adults around the world each year.

It is the most common cause of dementia in the elderly.

Despite this there is currently only one drug that has so far been approved for treating dementia.

The new vaccine, though, targets proteins that build up in the brain that are thought to be the cause of Alzheimer’s disease.

Professor Nikolai Petrovsky, who led the research, said:

“If we are successful in pre-clinical trials, in three to five years we could be well on the way to one of the most important developments in recent medical history.

Along with our rapidly ageing populations, we now know that the explosion in type 2 diabetes in the West is likely to further dramatically fuel the projected rise in the number of cases of dementia globally, with diabetes being the major risk factor for Alzheimer’s disease.”

The vaccine, which is called ‘MultiTEP’ fights both beta and tau amyloid plaques that are linked to Alzheimer’s.

Professor Michael Agadjanyan, another study author, said the advantage of the vaccine is that it…

“do[es] not induce potentially harmful auto-reactive cellular immune responses, while still generating antibodies that bind strongly to the amyloid and tau pathological molecules in brain tissue from AD patients”.

Dr Anahit Ghochikyan, another study author, concluded:

“This study suggests that we can immunise patients at the early stages of AD, or even healthy people at risk for AD, using our anti-amyloid-beta vaccine, and, if the disease progresses, then vaccinate with another anti-tau vaccine to increase effectiveness.”

Preclinical trials have now been completed and the next stage is human trials.

The study was published in the journal Nature: Scientific Reports (Davtyan et al., 2016).

Brain image from Shutterstock

Study did not see the same benefit for wines and spirits.

Light to moderate consumption of beer could decrease the risk of brain diseases like Alzheimer’s, new research finds.

The study looked at different types of alcohol intake — beer, wine and spirits — and the link to neuropathological signs of Alzheimer’s.

The study included data from 125 people in Finland who had died suddenly between 35 and 70 years old.

Their brains showed that those who drank light or moderate amounts of beer had less amyloid plaques.

Amyloid plaques are thought to be important in the development of Alzheimer’s disease.

Consumption of wines or spirits, though, was not linked to the amount of amyloid found in the brain.

This is not the first study to link alcohol intake with a lower risk of dementia.

Here is another study I reported recently:

“One drink a day (or less) for women and 1-2 drinks (or less) for men reduces the risk of developing dementia, a study has found.

It works out to between 8 and 14 drinks per week.

The study is one of the largest — and longest — to look at the connection between alcohol and dementia.

Over 3,000 people aged 75 or over took part in the research, which followed them for over six years.

The study found that those who drank moderately had a 37% reduction in the risk of developing dementia compared with those who did not drink at all.

The study was published in the journal Alcoholism: Clinical and Experimental Research (Kok et al., 2016).

Scientist around the world are reaching a new conclusion about what causes dementia and other neurodegenerative diseases.

An out of control immune system could be the underlying cause of Alzheimer’s and other neurodegenerative diseases, research finds.

There is now strong evidence that the body’s own immune system is causing cells in the brain to die.

Professor Robert Richards, who led the study, said:

“Dementia, including the most common form Alzheimer’s Disease, and related neurodegenerative conditions are dramatically rising in frequency as people live longer and our population ages.

[In the United States it] is predicting that by 2050 there will be almost double the number of people with dementia.

Currently we have no effective treatments to assist the millions of affected people, and these diseases are an enormous burden on families and the public health care system.”

Proteins called amyloid plaques were previously thought to be the culprits in Alzheimer’s, but the evidence is not strong enough.

Professor Richards said:

“Our interest in the body’s own (innate) immune system as the culprit began when we discovered that immune system agents become activated in a laboratory model of Huntington’s Disease.

Remarkably, researchers from other laboratories were at the same time reporting similar features in other neurodegenerative diseases.

When we pulled the evidence together, it made a very strong case that uncontrolled innate immunity is indeed the common cause.”

The immune system may malfunction as a result of various triggers such as toxins, genetic mutations or physical injuries.

Professor Richards said:

“We hope this new way of understanding neurodegeneration will lead to new treatments.

We now need to further investigate the immune signaling molecules, to identify new drug targets that will delay the onset and/or halt the progression of these devastating diseases.”

The study was published in the journal Frontiers in Neuroscience (Richards et al., 2016).

Brain image from Shutterstock

The other side of the drug is that it can also increase the chance of bleeds in the brain.

The common blood thinner Warfarin has been linked to increased dementia risk by a new study.

Warfarin is typically prescribed to help prevent clots and strokes.

However, the other side of the drug is that it can also increase the chance of bleeds in the brain.

Bleeds in the brain are linked to worse brain function over time and dementia.

The study involved people treated with the drug for atrial fibrillation, the most common form of arrhythmia.

Dr T. Jared Bunch, the study’s lead author, said:

“Our study results are the first to show that there are significant cognitive risk factors for patients treated with Warfarin over a long period of time regardless of the indication for anticoagulation.”

The study involved 10,537 people with no history of dementia who were followed up over 7 years.

Dr Bunch said:

“First, as physicians we have to understand that although we need to use anticoagulants for many reasons including to prevent stroke in AF patients, at that same time there are risks that need to be considered some of which we are only right now beginning to understand.

In this regard, only those that absolutely need blood thinners should be placed on them long-term.

Second, other medications like aspirin that may increase the blood thinners effect should be avoided unless there is a specific medical need.

Finally, in people that are on Warfarin in which the levels are erratic or difficult to control, switching to newer agents that are more predictable may lower risk.”

Naturally, anyone considering changing their medication should consult their physician.

The findings were presented at Heart Rhythm 2016 in San Francisco.

Image credit: cora alvarez

Hope for a general strategy against neurodegenerative disorders found.

A five-year study has identified a way of reversing the symptoms of diseases like Alzheimer’s and Parkinson’s.

The research on fruit flies involves inhibiting two key enzymes.

Professor Flaviano Giorginia, one of the study’s authors, said:

 “The two most common neurodegenerative disorders worldwide are Alzheimer’s and Parkinson’s disease.

The treatment options for these diseases are limited, and to date no cures exist.

Our hope is that by improving our knowledge of how these nerve cells become sick and die in the brain, we can help devise ways to interfere with these processes, and thereby either delay disease onset or prevent disease altogether.”

The enzymes targeted by the research increase levels of a key metabolite called kynurenic acide.

Professor Giorgini explained:

“There is a fine balance between levels of “good” and “bad” metabolites that occurs in the kynurenine pathway.

In disease, it shifts towards the “bad”, and by inhibiting TDO or KMO, we shift it back to “good”.

For example, we find that if we inhibit either TDO or KMO in Huntington’s flies we reduce loss of neurons.

In Alzheimer’s or Parkinson’s flies we see extension of the shortened lifespan exhibited by these flies, and we also reverse the defects they have in movement.

We have even used a drug-like chemical to inhibit TDO and found that this also alleviates ‘symptoms’.”

Professor Giorgini concluded:

“We are excited by these results, as they suggest that TDO and KMO inhibition could be a general strategy employed to improve symptoms in a myriad of neurodegenerative disorders, not just Parkinson’s and Alzheimer’s.

Indeed, five years ago we first showed that these manipulations could improve “symptoms” in Huntington’s disease model flies, so our next step is to validate our work in mammalian models and ultimately to see if such drugs could be helpful to patients in clinical trials”

The study was published in the journal Proceedings of the National Academy of Sciences (Breda et al., 2016).

Alzheimer’s image from Shutterstock