Published on: March 17, 2012
by Professor David smith for The Daily Mail
Modern medicine has let us cheat death. We can replace organs, take pills to stave off heart disease, cure many cancers, and control previously fatal conditions such as diabetes. As a result, the average life expectancy is 80, whereas 100 years ago it was 52. Yet now, if these other illnesses don’t get us, it seems that dementia will.
More than 800,000 Britons suffer from some form of the disease, with 75 per cent of them having Alzheimer’s. All lead to mental decline, memory loss, speech and movement problems, and death.
The world’s bestselling medication for Alzheimer’s (AD) is donepezil, marketed as Aricept until its UK patent ran out last month – and it’s now 80 per cent cheaper as a result.
But while donepezil improves memory function in patients with mild to moderate AD or with Mild Cognitive Impairment (MCI) – minor memory problems that may be a precursor to dementia – it helps only a third of full AD sufferers; others will get no benefit or suffer side effects.
For those for whom it works, the drug improves quality of life for a year or two. After that, since the brain damage caused by the disease progresses, patients may show a marked decline. Modest as its effects are, it is widely used because it is the best drug of its kind. But I believe if we are to beat this horrific illness, a more broadminded approach is needed.
It’s a folly that such huge amounts are pumped into searching for a ‘new Aricept’. While donepezil has had some success, countless other similar drugs have foundered.
The fundamental problem with Alzheimer drug research is that it is almost entirely based on the ‘amyloid hypothesis’, a theory about what causes AD that appears increasingly invalid.
Amyloid is an insoluble toxic protein deposited between the nerve cells of the brain that has been shown to kill them. In 1991, scientists in London discovered that a mutated gene in the precursor protein to amyloid (beta-amyloid) caused a rare genetic form of AD. Since then, drug companies have considered that manipulating amyloid lies at the heart of dealing with AD.
But this puts all their eggs in one basket. Billions of pounds have been spent, and every single trial has failed. Some drugs made the symptoms of dementia worse.
Research should be geared towards intervening at an early stage. This is key to slowing down or stopping nerve cell death associated with AD. Once the nerve cells have died and the brain has shrunk, it’s too late.
I am the founding director of the Oxford Project to Investigate Memory and Ageing (OPTIMA), which studies the causes of dementia. Last year we recruited 270 elderly people with memory problems and gave them Vitamin B tablets – folic acid (800 micrograms), B12 (500 micrograms) and B6 (20 milligrams).
The supplements, which cost as little as 10p a day, were found to slow shrinkage of the brain by an average of 30 per cent a year – and slow the rate of cognitive decline – in people with high blood levels of homocysteine. Raised levels of this amino acid can increase the risk of developing AD three or four-fold.
By regulating homocysteine with B vitamins, we showed for the first time it is possible to slow the progress of the disease, if you start early. More trials are needed to test whether continued treatment can delay its progress indefinitely, but B vitamins have been shown to be as good clinically as Aricept – and better in that they slow the disease progression rather than ease the symptoms.
There is no way of knowing who is predisposed to AD, apart from extremely rare familial forms of AD.
But those with memory problems should have their homocysteine measured and be started on B vitamins, under medical guidance. Normal dietary intake isn’t enough. One (200ml) glass of semi-skimmed milk contains 2.5 micrograms of B12, and most manage to eat five micrograms a day. But we do know people with high Vitamin B intakes are less likely to develop dementia, so every little helps.
Large-scale studies are needed to see if nutrition and exercise can slow the conversion of memory impairment to Alzheimer’s disease. We also need to know if they improve the response to drugs such as donepezil.
For OPTIMA, the next step is a trial of 1,000 people with MCI to see if B vitamins prevent the conversion to dementia over a two-year period. Can AD be beaten? I am optimistic.
The author is Emeritus Professor of Pharmacology at the University of Oxford and co-founder of OPTIMA.
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