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Now is the time to research Alzheimer’s

by Rowan Hooper

The team leader at the Laboratory for Proteolytic Neuroscience at Riken’s Brain Science Institute is not a man usually given to making apocalyptic statements.

Yet when I asked him whether Japan should be investing more money in Alzheimer’s research, he responded with more than the usual academic plea for more money. “Alzheimer’s disease,” said Takaomi Saido, “will destroy Japan’s social-welfare mechanisms in the near future.”

Saido, based in Wako, Saitama, is on a twin social and scientific mission: to protect Japanese society from the ravages of Alzheimer’s disease, and to uncover the secrets of how the brain ages.

It’s interesting that he emphasizes that his mission is about protecting society. Alzheimer’s is already one of the most expensive diseases in developed countries. In the United States, it costs more than $100 billion a year. Saido is only too aware of how this will increase.

“My social mission is to protect social-welfare mechanisms,” he told me, “because the socioeconomical cost of Alzheimer’s disease will be greater than the government’s annual income by 2050 unless the disease becomes preventable.”

That sounds like a lot of money. But the estimate for the financial burden caused by Alzheimer’s in Japan by 2050 is $500 billion a year, which is about the same as the government’s annual revenues. Why is the cost going to increase so much?

“People will be receiving much less pension after retirement and paying more taxes and hospital costs,” Saido said. So the government should invest now to save in the future. If we can find a way to treat or prevent Alzheimer’s, the number of people who suffer from dementia and the burden on caregivers will be smaller.

“Alzheimer’s research is much more cost-effective than any other research field, including stem-cell research,” Saido assured me.

As an example, Saido offered his new mice. Years in the making, these are no ordinary mice. The Riken team thinks it may revolutionize research into Alzheimer’s, and this is the scientific part of Saido’s twin mission. “My scientific mission is to uncover the essence of brain aging, one manifestation of which leads to Alzheimer’s disease development.”

Much of the research conducted into Alzheimer’s uses mice as “models” of humans. Scientists use strains of mice that have a genetic propensity to develop Alzheimer’s-like symptoms, and it might go without saying, but mice are not the same as people, and the models are not perfect.

In particular, the strain of mouse commonly used in Alzheimer’s research makes too much of a particular protein, known as amyloid precursor protein. This APP leads to the production of amyloid deposits, which are thought to cause the breakdown of neurons in the brain and which are the hallmarks of Alzheimer’s disease.

But since the mouse makes too much APP, Saido thinks much of the work done on that mouse strain — and there has been a lot — is flawed, and won’t help our understanding of the disease in humans. The new mouse model is a strain that produces APP and the subsequent amyloid deposits in a way that is more realistic for the actual human disease. The details have just been published in the journal Nature Neuroscience.

“The generation of appropriate mouse models will be a major breakthrough for understanding the mechanism of the disease,” said Saido, “which will lead to the establishment of presymptomatic diagnosis, prevention and treatment of the disease.”

I asked Saido for any preventative advice. “To my knowledge, the only scientifically proven measure is a daily exercise, like one hour of walking,” he said.

Much remains to be discovered about this insidious disease. But there is hope. Two recent papers in the British journal the Lancet show that in the U.K. and Denmark there is a decrease in the number of people getting Alzheimer’s disease.

The first paper shows details of two surveys of people with Alzheimer’s in the U.K., one in 1994 and the other in 2014. The researchers expected that the second survey would show more people with Alzheimer’s, since the average age of the population had increased over the intervening 20 years.

But the numbers came up some 200,000 short. The evidence suggests that people are developing Alzheimer’s at an increased age. Something appears to be delaying the onset of the disease. (The DOI reference for this paper is 10.1016/S0140-6736(13)61570-6.)

The Danish study shows that people in their 90s born in 1915 were healthier and smarter — they performed better on cognitive tests — than people in their 90s born in 1905. So something improved in the lifestyle or diet of people born in 1915 that seems to have protected them. (The DOI reference for this paper is 10.1016/S0140-6736(13)60777-1.)

What are we to make of this? Some might say that it shows, for developed countries at least, that better nutrition, fitness and education may be helping to reduce the reach of Alzheimer’s. Maybe that’s true — but only slightly. “To conquer Alzheimer’s disease, it is essential to establish presymptomatic diagnosis and preventive medicine,” said Saido.

He also suggests that the apparent decrease in Alzheimer’s seen in the U.K. may be due to a decrease in the consumption of fish and chips. That’s not as glib as it might seem, as an improved diet could reduce vascular forms of dementia, which would also reduce Alzheimer’s.

But even if you doubt that the fabric of society is at risk — or that fish and chips have much to do with it — he’s right that we need to conquer the disease.
