If you didn't know better, you'd think Alzheimer's disease is the plot of a bad horror movie: A creeping silent killer steals your memories, distorts your experiences of the present, and transforms your family's love into dutiful pity.
And like a figure lurking in the shadows, no one knows why Alzheimer's strikes. It is not quite random, as most people who develop it carry a single genetic mutation. And nobody understands why some people with the mutation develop Alzheimer's and others do not. Many scientists believe the cause lies in a combination of environmental factors: a series of chemical exposures, dietary choices, or bonks on the head. Two studies recently implicated diet and regular soda, suggesting that people who regularly consumed it had higher risk of dementia and Alzheimer's.
Given that personal genetics tests like 23andMe let people determine whether they carry this maybe-you-have-it mutation, findings of things like the soda study can lead to self-diagnostic panic. But don't drive yourself crazy worrying about this. Like most diseases, Alzheimer's is the things you can and cannot control. So ground yourself with knowledge about both the genetic and environmental (read: everything else) risks before the next wave of Alzheimer's hysteria.
The disease is named for a German doctor named Alois Alzheimer, who treated a woman named Auguste Deter for an assortment of strange psychoses. She experienced "strange feelings of jealousy towards her husband," followed by rapid memory loss, "dragging objects to and fro, hiding, or sometimes thinking that people were out to kill her, so then she would start to scream loudly." Intrigued, Alzheimer arranged to receive her brain after she died. Upon dissecting and dyeing layers of the shriveled organ, he identified microscopic tangles and plaques amid the grey tissue and in 1907 hypothesized that they had caused Deter's degeneration and death.
These tangles and plaques are familiar to doctors who study the disease. But they remain incredibly mysterious. Scientists know where they come from, but not how they come about. Tangles result from the breakdown of microtubules, nutrient highways in the brain that are stabilized by proteins called taus. Unable to distribute nutrients, the cell dies and collapses into a tangle. The plaques form when rogue enzymes snip so-called amyloid precursor proteins (which help neurons grow and repair themselves). These proteins crumple and harden into a plaque.
But ... why? The foundational clues come from genetics. The suspect behind most cases of Alzheimer's is a single mutated gene on chromosome 19 called apolipoprotein E epsilon-4. People who carry one copy of epsilon-4 (remember, everyone gets two copies of every gene, one from each parent) have up to a 40 percent chance of developing Alzheimer's. If both genes are epsilon-4, that risk can jump as high as 87 percent, says Susan Hahn, a genetic counselor specializing in Alzheimer's disease. "About 25 percent of the population has at least one epsilon-4 variant," says Hahn. "And only about 2 percent have two copies."
Another 2 percent of people carry one of three mutations that guarantee the disease---specifically, early-onset Alzheimer's, which hits decades earlier than the more common form of the disease. 23andMe is not allowed to show people if they carry those genes. If you have one of those genes, you probably know about your Alzheimer's risk already. These people come from families where virtually every member develops dementia. Many are participants in long term scientific studies.
But, say you took a 23andMe test and the results reveal that you have the gene variantepsilon-4, the big maybe? Should you quit drinking soda, move away from the freeway, or learn Mandarin?
Studies that warn of things like that describe environmental risks, not genetic ones. But those risks only suggest a probable statistical association between two things that have already happened: getting Alzheimer's and something else. The studies linking soda consumption to Alzheimer's used retrospective analyses: Researchers examined data collected over a long period of time. Such analyses are notoriously difficult to interpret.
In the first of the two soda studies---the one linking artificial sweeteners to stroke and dementia—that retrospective data came from something called the Framingham Heart Study, which started in 1948 with more than 5,000 participants. The original subjects, their children, and grandchildren have for decades completed periodic health exams and diet surveys. Looking back on this data, the researchers made the correlation between the sweeteners used in diet soda and diseases. What they did not do is connect the molecules from diet soda sweeteners to specific triggers inside the body, and track these triggers throughout the decades it would take to destroy a brain.
Functionally, those studies don't really tell you anything at all about whether or not you will get Alzheimer's. The combination of causes is too obtuse for any one lifestyle change to make a difference.
However, most of the lifestyle changes these studies suggest are good from any perspective: Soda (even maybe diet) is bad for you, freeways are polluting, and Mandarin looks great on your resumé. But as far as Alzheimer's, the disease remains so mysterious that Hahn questions whether 23andMe's updated risk service is even necessary. "The only useful thing people can do with this information is worry, and that's not very useful," she says. It's the kind of knowledge might drive you crazy.
