Earlier this month newspapers reported that Columbo—that is, actor Peter Falk—has Alzheimer’s Disease. Usually, when news breaks that a celebrity is suffering from a serious medical condition, there’s a flurry of coverage discussing the nature of the disease. Hopefully, the pattern will hold in Falk’s sad case—because Alzheimer’s is both a terrifying disease and a greater public health issue than most of us realize.   

Indeed, the incidence of Alzheimer’s Disease (AD), is rising. According to the Centers for Disease Control and Prevention, in 2006 Alzheimer’s disease was the sixth-leading cause of death in the U.S., killing 72,914 people. Another startling number: Alzheimer’s as a cause of death has skyrocketed in recent years, increasing by 33 percent between 2000 and 2004.

So What Is It?

A progressive brain disorder, AD literally shrinks the brain, eroding individuals’ memory, language, and their ability to coordinate basic motor skills like swallowing, walking, and bladder control. These deficiencies can lead to other serious problems: an inability to swallow can cause food to be inhaled, which can lead to pneumonia; not walking can lead to painful bedsores prone to infection; and incontinence can also lead to infections.

In other words, Alzheimer’s is a frightening disease that gradually can take over the mind and body.  Unfortunately, there is no known cure, and currently no medical tests that allow us to diagnose the disease with 100 percent certainty—doctors need to cut open the brain in order to tell for sure that it’s afflicted with AD.

Further, no one knows for sure what causes Alzheimer’s, though researchers do have some understanding about what happens to the brain during the disease. The culprits are two abnormal structures called plaques and tangles, which together kill nerve cells in the brain. Plaques build up between nerve cells and deposit proteins that impede normal neurological functions; tangles are knots of protein that build up in brain cells and collapse the structures needed to transport vital nutrients across the brain.  

Doctors aren’t entirely sure what causes the growth of plaques and tangles. Genes might play a role, but researchers don’t know just how—or how much—they matter. That’s due in part to the fact that Alzheimer’s, when it’s genetic, is not caused by a single gene, but rather mutations on multiple chromosomes. Sadly, this information is not as useful as it may seem: according to the National Institute of Aging (NIA), less than 10 percent of AD patients have “familial Alzheimer’s”, i.e. a genetically inherited form of the disease. Onset of familial AD is early, before the age of 65.  The other 90+ percent of Alzheimer cases are late-onset (after 65), and according to the NIA, this form of the disease “has no known cause and shows no obvious inheritance pattern.” Researchers have a hunch that genes play some sort of role in late-onset AD, but “only one risk factor gene has been identified so far” and it’s not enough to account for the entire disease.

Why Is It on the Rise?

Currently, there are about 5 million people with AD; by 2050, that number will hit 16 million, making for a more than three-fold increase—in a large part because there will be more people over the age of 65, when Alzheimer’s is most likely to hit. In fact, people over 85 are the fastest growing segment of the population, meaning the number of Americans at increased risk of the disease is growing quickly. And thanks to medical progress that has reduced death rates from other diseases, people are living longer than ever—which means they’re living long enough to be at risk for Alzheimer’s.  (Indeed, as Alzheimer’s-related deaths increased between 2000 and 2004, the number of deaths caused by heart disease, breast cancer, and strokes all decreased).

Another factor behind the rise in Alzheimer’s is the fact that researchers have expanded their definition of what constitutes an AD-attributable death. Before 1999, if someone with Alzheimer’s contracted pneumonia as a result of not being able to take care of themselves and died from the infection, their cause of death would be considered pneumonia. But in 1999, such deaths were reclassified as Alzheimer-caused, since it was AD that made them susceptible to the condition in the first place. This change partially explains sky-rocketing AD rates

It’s important to put AD in context. It’s still responsible for far fewer deaths than the diseases ahead of it in the mortality rankings. According to the CDC, in 2006, heart disease killed 629,191 people; cancer killed 560,102; respiratory diseases like emphysema and bronchitis killed 124,614; and unintentional injuries killed 117,748. In other words, more people died in an accident than died from AD.

Still, as America age older and researchers find Alzheimer’s behind more and more deaths—even when the immediate cause is sickness, frailty, or infections—our health care system will shell out more and more money to treat the disease. Indeed, the number of Medicare claims for treatment of Alzheimer's disease shot up by 250 percent during the 1990s and is expected to increase by 300 percent over the next 10 years. Further, Medicare spending on Alzheimer's disease is expected to triple from $62 billion in 2000 to $189 billion by 2015.

Risk and Prevention

The uncertainty surrounding the causes of Alzheimer’s is reflected in the confusion as to what does and doesn’t help to prevent, or reduce the risk of contracting, the disease. Reading through the literature on Alzheimer’s is like talking to a split personality.

A few years ago, some studies suggested that taking pain relievers such as Advil and Aleve could prevent Alzheimer’s because these anti-inflammants were thought to reduce the brain inflammation that may occur during the disease’s growth. Newer studies in Neurology and the British Medical Journal, however, argue emphatically that this is not the case. They note that “over-the-counter [remedies] and prescription pain reliever[s]…[do] nothing to prevent Alzheimer’s disease” and “that aspirin d[oes] nothing to prevent memory loss in older women.”

In 2000, a study in the Archives of Neurology suggested that statins cut the risk of developing Alzheimer's disease by as much as 73 percent; in 2007, University of Washington researchers discovered that the brains of deceased Alzheimer’s patients who took statins during life had fewer plaques and tangles than AD patients who didn’t take the cholesterol-lowering drugs. But in January of this year, a Neurology study declared that there was absolutely no connection between statins and Alzheimer’s. 

This most recent study tracked new cases of Alzheimer’s disease amongst a cohort of 929 religious officials. When the study started, the average participant was 75 years old. Only 13 percent were taking statins. Participants underwent regular checkups and took mental skills tests every year for up to 12 years. During that time, 191 of them developed Alzheimer's disease—and taking statins “didn't affect the odds of getting Alzheimer's disease or milder mental decline.” Further, statins didn't affect Alzheimer's-related brain plaque as observed in post-mortem autopsies. 

More backpedaling: a 2002 study from the Netherlands found that “one to three drinks of alcohol per day had a significantly lower risk of dementia (including Alzheimer's) than did abstainers.” Subsequent 2005 research from Saint Louis University strengthened this claim. But in 2008, another team of researchers from Florida’s Mount Sinai Medical Center found that people who have “had more than two drinks a day developed [Alzheimer’s] almost five years earlier than lighter drinkers.”

Clearly, there are still a lot of unanswered questions surrounding Alzheimer’s—but there are a few measures that have consistently been proven to help fight AD. One is mental activity that keeps brain functions sharp: a 2003 study from the Albert Einstein School of Medicine found that playing chess, checkers, or a musical instrument reduced risk of Alzheimer’s amongst a cohort of 469 people over the course of 21 years. Such activities either delay onset of the disease by strengthening mental faculties or “may even create new brain cells in areas affected by Alzheimer’s.”

The more formal long-term development of mental acuity—i.e. education—is also helpful. People with higher levels of education (at least 15 years) have consistently been shown to have a “cognitive reserve” of extra neural connections, which allows their brain to handle more plaques and tangles without showing Alzheimer symptoms. Conversely, “people who don't finish high school are at a higher risk of developing dementia and Alzheimer's disease compared to people with more education, regardless of lifestyle choices and [other] characteristics,” according to a 2007 study from Finland.

Another good bet is eating well and exercising. There’s a rapidly growing body of evidence that a Mediterranea
n diet (fruits, vegetables, beans, grains, nuts, olive oil and fatty fish) reduces Alzheimer’s risk by providing the body with a lot of vitamins E and C and omega-3 fatty acids. At the same time, high-fat diets (like fast food) have been linked to increased risk of Alzheimer’s.

With regards to exercise, a 2006 study from the University of Washington concluded that “regular exercise reduces the risk of dementia and Alzheimer's disease by up to 40 percent,” and exercise has been shown to reduce brain shrinkage in people in the early stages of the disease. In 2005, Dr. Ronald Petersen, director of the Alzheimer's Research Center at the Mayo Clinic, told ABC News that "regular physical exercise is probably the best means we have of preventing Alzheimer's disease today, better than medications, better than intellectual activity, better than supplements and diet." This is because exercise improves brain function by boosting blood flow to areas of the brain used for memory.

Next Steps

Given what we know—and what we don’t know—about Alzheimer’s, it is clearly a condition that’s waiting for a break through. But how to help this breakthrough along? It’ll be tough, thanks to the inherent difficulties of researching AD: the brain is a mysterious, complex thing, and researchers have a hard time dealing with the proteins related to AD because they have a unique, fluid structure.

On the other hand, it’s clear that we could be doing more to support Alzheimer’s research. In 2007, the National Institutes of Health allocated a paltry $644 million to AD research, as opposed to $2.9 billion to HIV/AIDS—which kills only about 22 percent as many people. Meanwhile, prostate cancer is responsible for only 38 percent as many deaths as is Alzheimer’s, but receives significantly more funding.

To a certain extent, these discrepancies probably have something to do with the power—or lack thereof—of advocacy groups surrounding particular diseases. NIH funding is appropriated by Congress, and part of this process involves allocating budgets to the NIH’s “sub-institutes,” each of which specialize in distinct fields, such as the National of Aging and the National Cancer Institute. As you can imagine, the Institutes that deal with higher-profile diseases tend to receive larger sums. In 2007, for example, Congress gave 4.6 times more money to the National Cancer Institute than it did the NIA—the federal government’s main source of Alzheimer’s research support.

In other words, Alzheimer’s is not near the top of the NIH funding hierarchy—and with 85 percent of the NIH budget going to supporting scientists at universities and medical centers around the country, this is important. Worse, total funding for the NIH has stalled under the Bush Administration: since 2003, NIH’s budget has remained essentially flat.

"Even as substantial advances appear within our grasp—including breakthroughs in Alzheimer's disease, lung cancer and depression—they are at risk of slipping away because the NIH is experiencing a dangerous slowdown in funding," warned a March report from a group of top universities including Harvard, Brown, Duke and UCLA.

The NIH is a particularly important resource for AD research because drug companies are dropping the ball when it comes to the disease. They’ve been too quick to peddle new treatments that just don’t work. This past summer, Wyeth Pharmaceutical admitted that a drug it was pushing as an AD wonder-drug “failed to show an overall benefit in cognitive function for Alzheimer’s patients”; in June, a genetics company called Myriad announced that there was “virtually no difference between the treatment group and the placebo group” in trials that it ran for its AD drug Flurizan. “I think we have seen companies rushing things a bit,” Rudi Tanzi, a neurologist at Massachusetts General Hospital, told the Wall Street Journal. “It’s because Alzheimer’s is such a huge medical need. Companies are rushing to get the first drugs out the door.” But first doesn’t necessarily mean best—or even effective.

In contrast to drug companies, the NIH takes a long-term approach to disease research, and it will likely play an important role in any Alzheimer’s break-through—as long as it’s allocating the resources it needs to investigate this mysterious, heart-breaking disease.