Health and Medicine
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Alzheimer’s disease was the seventh largest cause of death in the US last year. As life expectancies rise and anti-aging research looks to push humans past their natural limits, it will only exacerbate an existing problem – in fact, the number of cases is expected to double every 20 years until it hits an astonishing 139 million people living with dementia in 2050. Yet despite scientists’ best efforts, every single dementia drug fails.
The rest of this article is behind a paywall. Please sign in or subscribe to access the full content.Most recently, the long-anticipated drug crenezumab, which targets amyloid plaques, failed clinical trials, proving unable to demonstrate any significant improvement in people with inherited Alzheimer’s. Disappointment was widespread, yet those familiar with the field were unsurprised, jaded by years of similar results.
So, what is it about Alzheimer’s that makes it so hard to solve?
A number of ideas have been put forward. It may be that our animal models are inherently flawed: Mice that scientists engineer to have an Alzheimer’s-like phenotype might not actually have the disease (after all, it’s hard to tell whether animals have brain disorders at the best of times).
Alternatively, most research focuses on amyloid plaques, which are build-ups of mis-folded proteins thought to block signals in the brain. However, it remains without any definitive proof whether these plaques cause Alzheimer’s, or whether they exist simply as a consequence. All we know is that they are a clear feature within the brains of people with the disease and that they can cause neuron damage.
A shift in strategy
Now, a group of researchers are suggesting it may be time to shift focus away from creating a miracle drug that halts Alzheimer’s in its tracks, and instead turn our attention to things we do know, such as behavioral risk factors that have been proven to increase risk. High blood pressure, smoking, and hearing loss are all highly implicated in the development of Alzheimer’s, so what if policy shifted to prevention instead of cure?
That is the argument of a new study recently published in JAMA Neurology, which has found that a large number of dementia cases in the US could have been prevented if lifestyle risk factors were reduced, based on their findings.
Specifically, the study looked at 16,690 participants from across the US, including some data from Asian and Pacific Islander backgrounds, to assess risk scores of various behavioral traits. They then generated population attributable fractions (PAFs) for each risk factor, representing the percentage of US dementia cases that would be prevented if this risk was eliminated.
Hypertension came out as the clear leader, with a staggering 12.4 percent of dementia cases being preventable if hypertension was solved. Hearing loss also played a role with a more modest 1.8 percent, but when adjusted for the huge number of dementia cases across the US, this represents around 100,000 preventable cases each year if it was targeted with readily-available treatments.
According to one psychiatrist speaking to The New York Times, it is time we shifted policy towards preventing risk factors. Their work suggests that up to 40 percent of all dementia cases could be a result of 12 preventable or treatable lifestyle factors.
“A massive change could be made in the number of people with dementia,” said Dr Gill Livingston, chair of the Lancet Commission on Dementia prevention, intervention, and care.
“Even small percentages – because so many people have dementia and it’s so expensive – can make a huge difference to individuals and families, and to the economy.”
