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Well Thought Out

“They do not grow old as we (who are left) grow old” is a thought usually attributed to those who died in the First World War. However, after reading about the latest results of a clinical trial of solanezumab for treating Alzheimer’s disease, I mused that it might also be applied to those suffering from this terrible affliction.

The trial could offer a breakthrough, but what worries me about the results is that the only 100% diagnosis of the disease and its cause (amyloid plaques and tau tangles in the brain) continues to be based on post-mortem pathology of brain material.

Other tests, such as positron emission tomography, magnetic resonance imaging and single-photon emission computed tomography scanning, combined with detailed psychological testing over a period of years, give good but not definitive answers. They are also useful at ruling out further underlying causes of dementia (caused by gradual changes and damage in the brain) like Lewy bodies, interruption of the brain’s Well Thought Out blood supply, or rarer causes, including: depression, encephalitis and HIV-related infections, some brain tumours, Parkinson’s, a lack of vitamin B in the diet, a lack of thyroid hormone, or even head injury.

While the rarer causes may be treatable, or the progression of dementia caused by them slowed or halted, until now, no positive drug trial had been reported.

In this study, solanezumab was shown to stave off memory loss in patients with mild Alzheimer’s over the course of several years. The effects may have been barely discernible to patients or their families, and it is no cure, but the wider implications of the study results have been hailed as “hugely significant” because it is the first time any medicine has reportedly slowed the rate at which the disease damages the brain.

The drug, developed by Eli Lilly, had previously been tested in a larger group of patients with both mild and moderate dementia, but this earlier study appeared to end in failure in 2012. Yet, further deeper analysis seems to show that of 1,300 patients with mild dementia, those who had been placed on the drug showed a roughly 30% slower decline in memory and cognitive tests than those who had taken a placebo during the 18-month trial. To patients yet to suffer from devastating memory loss, or the profound changes to personality that come later, this may appear to be a fairly small difference. But the results suggest that the drug can work as long as it is given to patients early, and for long enough.

Questions remain, however: was the drug simply treating the symptoms, not actually delaying the loss of neurons in the brain that drives memory loss? To test this, Eli Lilly switched the half of the 1,300 patients who had been taking the placebo onto the drug as well, and the entire group was given solanezumab for a further two years. If the drug was just treating the symptoms, the placebo group would be expected to ‘catch up’ over time. However, the latest findings, unveiled at the Alzheimer’s Association International Conference, showed that the differences between the two groups were still there – a sign that the drug had made a genuine impact on the progression of the disease.

Today, nearly 44 million people worldwide have Alzheimer’s or a related dementia. Only one in four people with Alzheimer’s have been diagnosed, however incompletely. Current costs run into trillions of dollars and, as populations age, this can only increase. The prospects for effective, affordable treatments remain bleak: so prevention is the best policy – and perhaps the only policy. At one conference I attended, an eminent Japanese gerento-neurologist advocated prevention using exercise, diet and intellectual stimulation. My neighbour in the audience commented: “Sounds like a round of golf, a good lunch and a few hands of bridge to me.” Not a bad solution.

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