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A silver lining to the rising tide of dementia


We’re all familiar with the studies and news reports that present dementia as a ticking public health time bomb in the heart of the developed world. And while it’s true that global dementia rates continue to rise due to ageing populations, a new study suggests that the actual per capita incidence may be in long-term decline. In other words, while the brute number of people with dementia may continue to increase due to demographic changes, the chances of anyone in particular developing the disease are in fact diminishing.

The study, published in JAMA Neurology, measured incident dementia in a population sample of 1350 people over the age of 70 and without dementia at enrolment, between 1993 and 2015. Dementia incidence declined in successive birth cohorts. In those born before 1920, incidence per 100-person years was 5.09, which dropped to 1.73 for those born in the latter half of the 1920s.

The researchers from the Albert Einstein College of Medicine in New York identified a tipping point in those born after 1929, in whom dementia incidence started dropping significantly.

They say their results are broadly consistent with previous studies, which saw a drop-off in the incidence of dementia from around 1990. That would be around the time when those born after 1929 were entering their 60s, at which point age-related dementia becomes more prevalent.

But they say it’s not easy to tease out why the decline in dementia incidence has occurred. Some experts have pointed out that it correlates with a trend towards greater levels of education, but the researchers say that adjusting for education levels did not attenuate the decline in dementia incidence.

Another potential explanation is improved cardiovascular health. Vascular risk factors increase the odds of dementia and the incidence of stroke has declined in recent decades, just as management of cardiovascular risk factors have improved. The researchers say this could partially explain the decline in dementia incidence, but not totally. Improved nutrition is another possible explanation, unexplored by the study. For the moment, why the decline has occurred remains, to some degree, a mystery.

The study authors also found an increased prevalence in diabetes over the years of the study. Dementia is linked to diabetes so this higher prevalence may, in the future, serve to increase the rates of dementia.

They say more work needs to done to further elucidate what’s happening and whether the decrease in dementia incidence will offset the increase due to the ageing population.

You can read the study here.

The link between anticoagulation and dementia


Atrial fibrillation patients are much less likely to develop dementia if they are taking an anticoagulant, a large Swedish study has found.

Although the the increased risk of dementia in atrial fibrillation has been known for many years, until now it has been unclear whether anticoagulation modifies that risk.

The retrospective study is the largest yet to look at dementia and anticoagulation. It involved nearly half a million people, comprising everyone in Sweden who had been diagnosed with atrial fibrillation from 2006 to 2014, with a cumulative 1.5 million years of follow-up. The study found a surprisingly large number of people – 54% – were not taking an anticoagulant, the use of which is recommended to mitigate increased stroke risk.

But those who were on anticoagulation treatment had, on analysis, a 48% lower risk of developing dementia. The study results also suggested that the earlier a patient started on an anticoagulant, the less risk of developing dementia he or she had.

The researchers also found a greater effect in patients with higher risk of stroke according to their CHA2DS2-VASc score.

Despite previous suggestions that novel oral anticoagulants (NOACs) may be more effective at warding off dementia than warfarin, the researchers found no difference between the types of anticoagulant medications in dementia risk.

The researchers cautioned that because of the retrospective nature of the study, they could not demonstrate cause and effect. Randomised trials would never be done for ethical reasons, but given the biological plausibility of a causal effect, the results “strongly suggest” that anticoagulants protect against dementia, the authors said.

Other independent risk factors for dementia in the study were increasing age, Parkinson’s disease, earlier stroke and alcohol abuse.

Study co-author Dr Leif Friberg, an associate professor of cardiology at Stockholm’s Karolinska Institute, said the important implications from the findings were that patients should be started on anticoagulant treatment as soon as possible after diagnosis of atrial fibrillation and they should continue on the drugs.

“Doctors should not tell their patients to stop using oral anticoagulants without a really good reason. Patients start on oral anticoagulation for stroke prevention but they stop after a few years at an alarmingly high rate. If you know that AF eats away at your brain at a slow but steady pace and that you can prevent it by staying on treatment, I think most AF patients would find this a very strong argument for continuing treatment.”

Dr Friberg said atrial fibrillation patients often have a fatalistic view about stroke, thinking that either they’ll get it or they won’t. But they tend to be less fatalistic about dementia and are more likely to do what they can to ward off the disease. That may make risk of dementia a more compelling argument to ensure that patients stay on anticoagulation medication, Dr Friberg said.

You can read the study here.

Why some people get dementia and others don’t


New findings on resilience to memory loss have been presented at the World Congress of Neurology, which is currently being held in Kyoto, Tokyo.

The US-based 90+ study has been looking at the mental health of the oldest of the old since 2003, enrolling over 1,700 participants over the age of 90 along the way. Data showed that around 40% of study participants had a dementia disease, with women over-represented in that group.

However, there was surprisingly little correlation between Alzheimer’s pathology – typically a buildup of amyloid-beta protein plaques and tau protein tangles in the brain – and dementia symptoms.

“Interestingly enough, autopsies revealed that about half of the oldest-old without dementia have a high degree of Alzheimer’s neuropathology in their brains although they were mentally fit while alive,” says Professor Kawas of the University of California, a lead researcher for the study.

At the same time, among participants who did develop symptoms of cognitive loss, around half did not have typical Alzheimer’s pathology.

The findings mirror those from the work of Professor Carol Brayne, a leading UK dementia researcher who runs a brain bank and dementia epidemiology program at the University of Cambridge.

Professor Brayne has also found very little correlation between the classic features of Alzheimer’s disease and beta-amyloid accumulation in post-mortems on people who were well characterised before they died.

These findings are clearly significant for any research program hoping to banish dementia by targeting Alzheimer’s pathology such as amyloid-beta accumulation in the brain. But it also prompts the question of why some people are cognitively resilient to Alzheimer’s pathology – which may have genetic origins – while others aren’t.

The 90+ study shows that at least some of the difference is attributable to lifestyle. Participants who were resilient to cognitive loss tended to exercise more, drink more coffee, and watch less television.

In a phenomenon known as cognitive reserve, higher levels of education seemed to protect against cognitive loss in people who were shown on PET scans to have amyloid plaque in the brain.

“People with a low level of education had a four times higher statistical risk of contracting dementia than those with a higher level of education. Among those without plaque, the educational difference was irrelevant,” says Professor Kawas.

The researchers also found that one of the best predictors of dementia was having multiple comorbidities.

“Multiple pathologies are at the root of dementias of all ages,” says Professor Kawas. “In the oldest-old, the presence of multiple pathologies is associated with increased likelihood of dementia. The number of pathologies also seems to be relevant for the severity of the cognitive decline. We will therefore need to target multiple pathologies to reduce the burden of dementia.”

Despite these advances in our knowledge of the causes of dementia, there remains great uncertainty over what preventive measures should be taken. The best evidence is for physical exercise, with studies showing that it can play a role in postponing or slowing age-related cognitive decline. High blood pressure in middle age has also been shown to be associated with later cognitive decline. And given the findings on cognitive reserve and dementia, cognitive training may also have an effect, but studies have yet to show this.

A new report acknowledges that more research needs to done on the efficacy of preventive measures, but suggests diabetes and anti-depression therapies, lipid-reducing drugs, initiatives to improve sleep quality and social involvement, and addition of folic acid to the diet along with other nutritional interventions may all be of benefit.

Access abstracts from the World Neurology Conference here.

Dementia study debunks exercise theory


Look at any of the multitude of articles of the past few years on how to avoid dementia and you’ll almost certainly read that exercise delays onset. Not so, according to the most recent research, published this week in the BMJ.

The 28-year study followed over 10,000 middle-aged British civil servants, noting at seven-year intervals whether participants were doing the “recommended” amount of exercise, defined as moderate or vigorous physical activity for 2.5 or more hours per week.

Surprisingly, the researchers found no correlation between how much exercise a patient did and whether they experienced cognitive decline over the study period, identified through a battery of cognitive tests, along with dementia diagnoses from hospital and mental health services.

The finding runs counter to several recent meta-analyses of observational studies which concluded that physical activity is neuroprotective in cognitive decline and dementia risk.

What the researchers did find was that in participants who eventually developed dementia, a decline in physical activity started around nine years before diagnosis.

This finding could be key to why previous observational studies have found a correlation between exercise and dementia risk, say the French researchers from the Centre for Research in Epidemiology and Population Health in Paris.

It’s now well known that brain changes start happening many years before dementia symptoms become apparent, and a decrease in physical activity is probably part of the cascade of changes in this preclinical phase of dementia, the researchers say.

The upshot is that findings of a lower risk of dementia with exercise may be attributable to reverse causation – in other words, decline in physical activity is due to the dementia, and not the other way around.

The researchers say that two problems with some of the earlier observational studies were that their duration was too short and their participants were too old. This made them more liable to be confounded by participants with preclinical dementia, who for that reason had lower levels of physical exercise.

They also point out a difference between observational and randomised trials, with the latter less likely to find a protective effect with exercise.

The recommendation of exercise for the prevention of dementia has already become enshrined in a number of international guidelines, including in Australia.

You can access the study here.