At the recent meeting of the European Academy of Neurology in Copenhagen, doctors were signing up to attend a workshop teaching non-specialists to test for cognitive decline in their patients. How do you tell the difference between a scatterbrain and a case of early dementia?
It’s a question that is increasingly urgent. Last year, 47.5 million people were living with dementia. That will have risen to 75.6 million by 2030 and will reach 140 million in 2050. The World Health Organisation has declared that dementia should be regarded as a global public health priority. But what can we do about it?
The primary cause of dementia, accounting for roughly 70 per cent of cases, is Alzheimer’s disease. It’s all very well to put a name to it, but we don’t have a clear understanding of the mechanisms that cause it – or medicines to battle it. Alzheimer’s drugs have a high rate of failure. In the decade to 2012, 99.6 per cent of newly developed drugs failed to make it past clinical trials. There is no cure for Alzheimer’s and none on the horizon, either.
There was, however, a small breakthrough last month. A study published in the journal Science Translational Medicine suggests that Alzheimer’s could be a result of fighting infections from other diseases that would, if left unchecked, ravage the brain. The hard lumps of sticky plaque in the brain that characterise the onset of Alzheimer’s seem to be the result of the immune system attempting to isolate and neutralise microbes and other pathogens that have made their way into the brain. The plaques catch pathogens, preventing infection from taking hold. Unfortunately, it’s a case of damned if you do, damned if you don’t: the plaques also trigger inflammation that leads to the death of brain cells.
This observation mirrors another catch-22 with Alzheimer’s. Some researchers have suggested that the drug failures might be averted by getting candidate treatments to the disease earlier, before symptoms appear. Put simply, the drugs may stand a better chance of success when trying to counter the first stages of damage to the brain. The problem is: how do you get that early diagnosis?
There are various genetic indicators for a heightened predisposition to developing Alzheimer’s. A gene called apolipoprotein E, for instance, comes in three variants: one kind seems to reduce the risk of Alzheimer’s while another increases it. Other genes – variously associated with the body’s uptake of cholesterol, its propensity to engender inflammation and the efficiency of communication between neurons – also have a role to play in raising or lowering the chances of onset.
However, the interplay between genetic factors, environmental factors and what appears to be pure luck makes foreknowledge of whether Alzheimer’s will strike any individual impossible. It’s no wonder that the US National Institutes of Health does not generally recommend genetic testing as a worthwhile route for anyone wanting to know their future. After all, a result that indicates you are more likely than the average person to develop dementia is, in many ways, little more than a heavy psychological burden, to be borne until the symptoms start to appear – a scenario that keeps you stressed (a grave health risk) even if onset never happens. If the drugs don’t work yet, why would anyone sign up to be tested?
In the absence of a reliable test or cure, the best advice seems to be to delay ageing as much as possible, particularly where cardiovascular health is concerned. It’s an observation that fits with last month’s breakthrough. The plaque-provoking pathogens reach the brain through the weakening of the blood-brain barrier, a wall of cells that wraps around blood vessels and prevents foreign bodies from passing into the brain’s circulatory system. This weakening happens with age, suggesting that action to delay the degradation of the cardiovascular system will also delay the onset of Alzheimer’s disease.
Here, at least, we have some good news: the rate of appearance of dementia cases seems to be in decline. This may be a spin-off of our attempts to cut deaths from heart disease. It seems that as we take control of blood pressure and cholesterol levels, making significant improvements to our heart and circulatory function, we are unwittingly improving our cerebral health, too – almost certainly because the brain requires good blood flow to operate well.
The surest way to avoid Alzheimer’s, then, is simple to state and impossible to achieve. All you have to do is stay young.
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This article appears in the 04 Jan 2017 issue of the New Statesman, Divided Britain