Myths and Facts about Alzheimer's

  • 24 Aug 2015
  • Reading time 11 mins
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Have you had one of those nasty moments recently when it is clear that your memory is failing? Confidently rushing up stairs to get something then realising you have no idea what it was? Meeting someone you know perfectly well and being unable to remember their name? A few of these moments and a name that none of us forgets comes all too easily to mind: Alzheimer’s.

Very scary since, as everybody knows there is no cure and nothing really to be done to prevent this horrible disorder. And there are other myths that you are probably aware of. Just give the drug companies a bit more time and money and they will come up with a cure. Another is that the two villains responsible, which can be targeted, blocked or destroyed, are a couple of damaged proteins found in sufferers brains – amyloid plaque and tau tangles.

However it is extremely unlikely there will ever be a drug “cure” because once brain cells are destroyed, no drug is going to bring them back. Drugs block things, they don’t regenerate brain cells. But surely some people are genetically doomed to develop the disease, so what about targeting genes? Another blind alley unfortunately since genes only account for 1% of cases of Alzheimer’s. 1

However there is reason to believe that at those moments when the word ‘Alzheimer’s’ pops up, the next thought shouldn’t be ‘despair’ but ‘prevention’. Despite the defeatist attitude of the charities and the understandable lack of interest by the drug companies, there are actually a number of sensible and plausible steps to take that have a chance of cutting your risk by half.

This was the powerful message set out in a statement by 112 leading dementia experts, delivered to the G8 summit on dementia in London in December 2013. It claimed that half of the risk of developing the disease is attributable to known risk factors and recommended that: ‘Health authorities should aim to identify high risk individuals at an early stage, when intervention is likely to help.’ Adding that: “There is already sufficient evidence to justify immediate action.’

The steps they mentioned included controlling blood sugar and blood pressure, taking exercise, cognitive training, social activities, and supplementing with omega-3 fatty acids and B vitamins. This statement has since been published in the Journal of Alzheimer’s Disease. 2

Unfortunately the health authorities, even when they are officially committed to “public health”, have so far proved pretty inept at changing the nation’s diet and lifestyle. The response of UK health minister Jeremy Hunt to the looming crisis, for example, has not been to announce funding for a national prevention programme on a scale that matches the 50 per cent that diet and life style contributes to the risk but instead to pledge to speed up the diagnosis of dementia from 6 months to 6 weeks. Far too little and far too late. Since 2006 the total spend on prevention research by UK health councils has been £156,000 – 0.1% of dementia research funding. With nothing else on offer those at risk must be identified much earlier and helped to make changes that could reduce it. The reality is that serious action to address the leading cause is effectively non-existent. How demented is that?

Homocysteine and B vitamins

So given that you are unlikely to get any support from drug companies, charities or health ministers to reduce your risk along the lines suggested by those 100+ experts, what can you do? The first course of action is to check out a third marker for Alzheimer’s, along with plaques and tangles, that is almost never mentioned – a high level of a potentially toxic amino acid called homocysteine, which is one of the best early predictors of risk

It is simply a statement of fact to say that billions have been spent targeting amyloid and tau because that way lies patents and profits. The only way to lower homocysteine, by contrast, is with high doses of B vitamins which are not going to make anyone a fortune. That’s why this approach needs public investment. Already it has far more evidence for effectiveness than anything the drug research has come up with. A dozen phase three trials of amyloid protein drugs have failed, some with quite disastrous side-effects. 3 Tau protein drugs have also failed, but there are more in the pipeline.

However there have so far been five randomised controlled trials of homocysteine lowering and each one has been extremely promising. Three came from the OPTIMA project at Oxford University treating patients with Mild Cognitive Impairment, a precursor to Alzheimer’s.

Memory decline almost stopped 4, shrinkage of the whole brain dropped by half 5, and shrinkage in areas that are specifically affected by Alzheimer’s was cut by an astonishing 88%. 6 A Chinese study found a drop in cognitive decline in patients with mild Alzheimer’s who had high homocysteine 7, while US researchers reported that memory decline virtually stopped in response to the vitamins among mild Alzheimer’s patients, but they didn’t measure homocysteine levels.

What all this suggests is that raised homocysteine is almost certainly causing memory problems and isn’t just a marker for raised risk. A number of highly plausible mechanisms have been identified that explain why raised homocysteine would lead to brain shrinkage, such as the fact that high homocysteine leads to the formation of amyloid plaques and tau tangles. 9

These results are hugely encouraging in their own right but they are even more important in light of what we know about levels of homocysteine and B vitamins in older people, the ones who develop Alzheimer’s. To begin with approximately half of people over 65 have raised levels of homocysteine and we know that their risk of accelerated brain shrinkage and Alzheimer’s is about four times higher than those with normal levels. We also know that having a raised level of homocysteine is linked with more amyloid and tau and that low levels of B ......

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