GIVING THANKS FOR LESS DEMENTIA
If, like me, you’ve been clawing urgently through recent events trying to find reasons to be thankful this Thanksgiving weekend, here’s a big one: As Star Lawrence observes at HEALTH’Sass, “Dementia decreasing–let us give thanks.”
Dementia has dropped dramatically in just a dozen years: from 11.6% of US adults over 65 in 2000 to 8.8% (and even a little lower, to 8.6%, among those over 85) in 2012. See Sharon Begley’s brief summary at STAT. The paper, free to read, was published by JAMA Internal Medicine on Nov. 21.
Because the US dementia rate plunged after 2000, the researchers said, more than a million people who would have been affected have been spared.
“Dementia” is an umbrella term for loss of memory and thinking and problem-solving ability, often accompanied by startling personality changes. As Trevor Plunkett emphasizes at the BMJ Blog, dementia is not a disease. It is a symptom of disease, and varies with the disease.
Alzheimer’s disease is probably the highest-profile disorder manifesting dementia. But dementia can be a feature of other brain conditions, such as Parkinson’s disease. An estimated 1 out of 3 cases of dementia are due to blood vessel diseases. These include arteriosclerosis (the accumulation of plaque in arteries) and atherosclerosis (artery stiffness with increasing age) that block the oxygen-rich blood brain cells must have to survive.
As Julie Corliss explains at the Harvard Health Blog, dementia can result also from strokes that block blood flow and kill off brain tissue, including the very common “silent” strokes, small blockages deep within the brain. Loss of cognition seems to be more characteristic in Alzheimer’s, while loss of memory often accompanies vascular disease.
Chronic diseases like diabetes and cardiovascular disease (especially high blood pressure) are risk factors for dementia. Those conditions are increasingly likely to be treated, which may be one reason the dementia rate dropped.
But reports on this paper, like Ina Jaffe’s at Shots, often emphasized another factor, one that seems to reduce dementia risk: education. The more you have, the less likely you are to develop dementia. Study subjects in 2000 averaged 11.8 years of education. By 2012 the average, 12.8 years, included a bit of college.
Is this an example of correlation being interpreted as cause? Maybe not. One theory is that education increases “cognitive reserve.” It forces the brain to make more connections. The more complex our brain networks are, the more easily the brain can resist damage by finding ways around it, as Anna Almendrala explains at the Huffington Post.
Her post describes the study methodology, noting that this is not the first research to show that dementia has declined. It is the largest though, involving 21,000 people over 65. “We’re definitely not certain or even confident that the declining risk we saw over the last 25 years will continue to decline, level off, or start ticking back up,” the lead researcher told her.
WHICH BRINGS US TO THE BAD NEWS
In these parlous times, there was bound to be bad news. So, despite the percentage drop, an estimated 5 million people in the US are affected by dementia right now, and the numbers are inevitably increasing. An estimated 14 million in 2050. And, gulp, 131 million worldwide. The US estimates are driven by the fact that the oldest members of the big post-WWII Baby Boomer population bulge have begun to turn 70. Dementia risk increases with age.
AND MORE BAD NEWS
Which brings us to the latest flop of a miraculous drug–about a hundred potential ones have been studied so far–for Alzheimer’s disease.At In the Pipeline, Derek Lowe is definitive: “After years of work and untold amounts of money, Eli Lilly’s Alzheimer’s antibody, solanezumab, does not work. It does not help Alzheimer’s patients. No matter how many times you run the Phase III trials, or in which patient populations, they do not get better. No matter how many hopeful press articles you might have seen on its prospects and no matter how many statementsyou might have seen from the company itself, no matter how you may try to spin the results, it does not do anything useful when you give it to actual Alzheimer’s patients. The program is over. It is done, because it does not work.”
(Side note on the In the Pipeline blog. I completely missed the fact that it moved to Science Translational Medicine more than a year ago. Lowe, a medicinal chemist, notes modestly that his reliable and illuminating blog, which focuses mostly on pharma, is one of the oldest science blogs, perhaps even the oldest, having been started in January 2002. “I have never once worked on any compound that has made it all the way to the market, not in 26 years and counting. If you want to know how come your prescriptions cost so much, it’s me.”)
Alison Abbott and Elie Dolgin try to keep hope alive in a post at Nature News, arguing that the drug’s death doesn’t mean that the amyloid hypothesis of Alzheimer’s disease is dead too. The amyloid hypothesis is the idea that Alzheimer’s results from amyloid protein buildup in the brain, known as plaques. Solanezumab is an antibody that seeks and destroys amyloid in blood and cerebrospinal fluid.
Maybe, they suggest, solanezumab would work if you just gave it to patients earlier. . .
But the fact is that the future of solanezumab–and other amyloid-targeting drugs–has been doubtful for a while. See the On Science Blogs post from July 2015. There I noted, “Recent research is also showing that even if a splendid Alzheimer’s drug arrives, it may be splendid for only part of the population, owing to human diversity.”
Despite these continuing disappointments, will the hunt for a magic bullet against Alzheimer’s disease continue?
You bet.
Medicare is now spending around 20% of its funds on caring for Alzheiemer’s patients. Not to mention that the profit potential is ginormous.
http://blogs.plos.org/onscienceblogs/2016/11/25/dementia-risk-declines-big-news-for-alzheimers-parkinsons-stroke/
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