In a little more than 15 years, the oldest baby boomers will start to turn 85.
As the boomers reach their “oldest old” years, the current trickle of long-term care insurance claims could turn into a silver tsunami of home care, adult day care, assisted-living facility, nursing home and hospice bills.
Or, medical research could do for the boomers’ long-term care services needs what it did for their tuberculosis care needs, and, eventually, for their polio, measles and mumps claims: Wipe them out.
Today, congressional committees are asking long-term care insurance specialists tough questions about why premiums have been increasing so rapidly.
In 30 years, if all goes well in the lab, lawmakers with no patience for history might be asking insurance company executives angry questions about why their companies have charged boomers so much money for insurance that covers a type of care that hardly anyone needs.
In the United States, the National Institute on Aging is the scientific body in charge of making the idea that older people often need years of labor-intensive care toward the end of their lives sound as strange to the health policymakers of the 2040s and 2050s as the idea that many children used to die of smallpox sounds to us.
The NIA, an arm of the National Institutes of Health, conducts and supports research on aging, and on the health of older people. It funds many studies on Alzheimer’s disease and other forms of dementia. It also pays for research on other conditions that can force older people to rely heavily on paid caregivers, such as Parkinson’s disease and severe arthritis.
The NIA recently summarized the state of dementia research in a “bypass budget,” or funding wish list, it sent to the White House and to Congress. In the document, officials talk about some types of research projects that long-term care planners might find very interesting. Officials talk, for example, about efforts to understand the epidemiology of Alzheimer’s disease, or just how many people will eventually have the conditions.
Researchers have already discovered something of obvious value to insurance underwriters: That people who are overweight when they are 50 seem to be noticeably more likely to have Alzheimer’s when they are older than other people.
The NIA wants to use some of any extra federal money the NIH gets to pay to put wearable sensors on the participants in existing federal health survey programs, and to supplement the results from questionnaires and quick medical exams with analysis of the participants’ genes.
The NIA also wants to expand support for research on the best ways to help people with Alzheimer’s stay in their homes, and to develop and improve methods for measuring dementia.
But the part of the bypass budget that seems the most exciting is the description of the Category A projects, or projects dealing with the “molecular pathogenesis and physiology of Alzheimer’s disease.” Those are the projects that could turn up new information that scientists could use to relegate Alzheimer’s disease to the medical history museums.
The most important Category A projects will lead the way for Category C projects, or projects to treatments and preventive measures into actual use.
For a look at five major strategies the NIH funding recipients included in the NIA bypass budget are pursuing, read on:
PICALM proteins might help a brain filter out amyloid plaque proteins. (Image: National Institute on Aging)
1. Using PICALM protein sponges to soak up Alzheimer’s wax
One team in the NIA report looked to see whether the PICALM gene really has anything to do with Alzheimer’s.
Cancer researchers and diabetes researchers had been running into the gene from time to time since the early 1990s. The authors of a purely statistical study reported in 2009 that the gene also seemed to have a connection with Alzheimer’s.
Last year, an NIH-funded team used new tools to figure out why the gene has a connection with Alzheimer’s: It seems to be involved with creating protein sponges that pull beta amyloid, the waxy protein that coats the brain cells of people with Alzheimer’s disease, out of the brain.
Researchers now want to see if putting more PICALM protein sponges in the brain helps people with Alzheimer’s disease function better.
Today, scientists can use cheap, fast DNA sequencers to detect and track the microbes hidden in people’s bodies. (Image: Thinkstock)
2. Looking at sneaky microbes
In the past, scientists who wanted to study how bacteria, viruses and other microbes affect human health usually had to figure out how to see the microbes with a microscope in a lab, and, in many cases, had to figure out how to grow the microbes in a lab.
Many of those microbes were hard to find, hard to see with a microscope and hard to culture in a petri dish.
Scientists now have a new strategy: They can use the same gene sequencers that help them read people’s chromosomes, or the strands of DNA that serve as people’s software, to read the DNA of any microbes that happen to be inside people’s bodies.
Scientists are discovering that the microbiomes, or collections of microbes, inside people’s bodies vary dramatically from person to person and seem to have a big but complicated relationship with health.
The NIH is already funding studies that use gene sequencing machines to identify human genes that might have something to do with Alzheimer’s.
The NIA wants the NIH to use extra cash it gets from Congress to pay for studies of the relationship between the microbiome, aging and dementia.
Researchers know a lot about beta-amyloid, a waxy protein that coats the brain cells of people with Alzheimer’s disease. Now they want to know more about beta-amyloid’s sister protein. (Image: National Institute on Aging)
Many scientists think beta-amyloid hurts the brain cells of people with Alzheimer’s. Some scientists think the beta-amyloid is simply the product of the brain’s effort to deal with some other problem, and that scientists need to figure out what that other problem is.
One thing that scientists on both sides of the beta-amyloid debate have noticed is that beta-amyloid has what amounts to a sister protein: amyloid precursor protein intra cellular domain, or AICD.
The mother protein is amyloid precursor protein, or APP.
APP breaks up to form the famous beta-amyloid protein and the much less famous AICD protein.
Researchers have found that, in mice, adjusting how AICD works affects how much beta-amyloid wax coats mouse brain cells. The NIA wants to fund studies to see whether working with AICD might be a way to reduce beta-amyloid levels in the brains of people with Alzheimer’s disease, and whether that makes those people healthier.
In some people, astrocytes may be to the brain cells people use to think roughly what poorly trained guard dogs are to the legs of letter carriers. (Image: iStock)
4. Astrocyte calming
Astrocytes are like attack-dog brain cells. When they see something that looks like an enemy, such as a poisonous protein, they shoot off weapon proteins.
NIH-funded researchers included in the NIA report tried exposing ordinary brain cells to astrocytes for two weeks.
Ordinary health brain cells have “dendritic spines and branches” that make them look hairy.
When astrocytes shot weapon proteins at the mouse brain cells in those study, the mouse brain cells lost some of their “hair.”
The researchers then gave mice with have dementia a drug, or “receptor blocker,” that protected the “hair” on their brain cells from the astrocyte weapon protein. The drug seemed to improve the ability of the mice to remember and learn, NIA officials say.
“This study heightens interest in developing such receptor blockers to treat Alzheimer’s disease,” officials say.
SIRT3 may protect people against Alzheimer’s disease by strengthening the batteries inside their brain cells. (Image: Wikimedia Commons Public Domain)
All animal cells, including human brain cells, contain tiny batteries called “mitochondria.” Scientists believe that problems with mitochondria might have something to do with many health problems.
In an NIH-backed study published earlier this year, scientists looked at the effects of SIRT3 on brain cell mitochondria.
SIRT3 is an enzyme that affects how cells read and act on the information in DNA. In the new study, researchers found SIRT3 helps keep mouse brain cell mitochondria healthy.
Physical exercise pumps more SIRT3 into mouse brain cells, and that could be one reason why exercise seems to prevent dementia, officials say.
The research suggests that finding other ways to increase SIRT3 levels in the brain might be a good way to fight aging-related brain diseases, officials say.
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