A very interesting article in the Guardian newspaper today

Detecting dementia: the first steps towards dignity

While we are a long way off a cure for dementia, new techniques might help us in the drive to identify it earlier, explains Tania Browne

   

    

PET scans of the brain of a normal patient (left) versus an Alzheimer's disease patient. The scan on the right shows reduction of both function and blood flow in both sides of the brain, a feature often seen in Alzheimer's. Photograph: PR

As a teenager, I lost my grandfather. But he wasn't dead. He still had his favourite music, he still loved to walk in the woods and name the flowers and plants, and he loved his soap operas. He was alive, but gone. A dignified man, a former aircraft engineer and oil company salesman, reduced to the status of a bewildered toddler lost in a shopping centre. When he died, our family felt an odd mix of relief, then guilt at the relief. The man we loved had left his body years before the body gave out.
This was 30 years ago. But while a cure is still far away, two new techniques may at least be able to forewarn us of dementia, and allow us to plan treatment for ourselves or loved ones before any outward symptoms are apparent.
According to Alzheimer's Research UK, my experience is currently shared by 24m relatives and close friends of the 800 000 diagnosed dementia sufferers in the UK. In December last year, a G8 summit was told by Alzheimer's Disease International that the worldwide figure was 44m and set to treble by 2050, as the life expectancy of people in middle and lower income countries soars – precisely the countries who have either depleted or non-existent healthcare systems. Dementia is a serious time bomb.
“Dementia” covers about 100 conditions, all resulting from large scale brain cell death. People often think that when they're diagnosed they're in the early stages. Yet cell death can be occurring for 10-15 years or more before any outward symptoms occur, and by the time they're diagnosed many dementia patients have already lost one fifth of their memory cells. Dementia affects language, your judgement and your general sense of who and where you are, among other things. The most common form of dementia is Alzheimer's, accounting for about two thirds of cases, but it's currently impossible to detect what form of dementia someone has while they're alive. The behaviour of all dementia patients is much the same, and we can only narrow it down to specific kinds by examining the brain after death.
Anyone interested in population health will tell you that no disease has a single cause. Epidemiologists work with many risk factors – factors linked with the likelihood of getting a disease – in the genetic, behaviour and environmental realms. Generally health conditions occur as a result of all three in various proportions, but in the case of dementia nobody knows. It's like having a recipe where the three main ingredients are given, but nobody has told you how much of each, what methods to use, and that each oven is completely unique.
This also makes developing treatments hard. The last drug, Memantine, was approved in 2003. Two more recent drugs have failed to show a significant result in clinical trials. There is hope that one of them, Solanezumab, may help delay onset in mild cases of dementia, but much research still needs to be done.
Although we don't know what causes dementia we find similar patterns in the brains of sufferers, and two proteins seem particularly significant. Proteins are made of long chains of amino acids, each of which needs to be in exactly the right place so the protein can fold up into a complex, particular shape – a bit like genetic origami. It's their unique shapes, and the fact that they can only attach to very specific receptor sites in the body, that make these proteins the key to so many essential body functions. So if something goes wrong, the genetic message mutates over time and a chain doesn't fold up the way it should... well, it's rather like folding up your beautiful origami swan and realising the instructions have told you to make three wings – except with genes you can't change or ignore the instructions.
In dementia patients, two proteins in particular are always found to have mutated and “folded wrongly”. One, called tau, is found all over the central nervous system where it has a role in stabilising microtubules, but it seems to be “tangled” in dementia patients. In September 2013 scientists at the National Institute of Radiological Sciences in Japan devised a chemical which could “bind” to tau and then be detected in the brain using a PET scan, and it's hoped this may also show effects on tau in future clinical trials.
But PET scans are still expensive and complicated, and the cheapest and simplest testing may be in searching for the second important protein, beta amyloid. This protein has several roles in the body, but where it forms part of the brain fluid, it can fold wrongly, tangle and cause a layer of “plaque” to build up. It's thought that the protein mutation may also bind with insulin receptors and prevent glucose from being properly absorbed in the brain, reducing function even further.
But it's been found that because it plays multiple roles, “clumps” of beta amyloid in the brain are mirrored by “clumps” elsewhere, specifically the lens and retina of the eye where it can be detected through bio-markers which bond with it. Two separate studies, from the US and Australia, were presented at the Alzheimer's Association Conference in Copenhagen last week, which showed that levels of beta amyloid in the eyes mirrored those in the brain. The results are preliminary and the tests have not yet been done on enough people to be sure, but in this early stage it looks promising.
So just as your regular eye test can provide early warning signs of glaucoma, it's possible that in future your optician may be able to refer you for further tests for signs of dementia. And the earlier we can detect dementia, the earlier treatment interventions we can make to plan treatment and to slow the progress of the disease. It may not be the “cure” for dementia, but it may well give us the first step to providing patients with maximum independence and dignity for the longest time.