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The Slow Fade
Last November the U. S. Food and Drug Administration issued a warning letter to 23andMe, the Mountain View, California, genetic testing firm that, for $99 and a cheek swab, would supposedly suss out your inherited risk for dozens of diseases. Some of the sussing was based on thin evidence, not on strong, proven links between particular genes and illnesses, and the company agreed to stop making health claims in its test results; pending further discussions with the FDA, the information will focus strictly on ancestry. That’s a bummer if you’re curious about your risk of developing Alzheimer’s disease, for which the company’s analysis was based on reliably solid data.
Not that DNA ever tells the whole story. Though you do have a higher risk of developing Alzheimer’s if it runs in the family, one person may begin manifesting symptoms in her fifties, while another may start to show signs only in his seventies. There’s growing evidence that lifestyle can play a role in delaying the onset of Alzheimer’s, perhaps enough to fend it off for years, and that may be a big reason why the rate of death from Alzheimer’s in L.A. is 16 percent lower than the national average, according to calculations based on U.S. Census and L.A. County Department of Public Health statistics.
In L.A. County some 160,000 people live with Alzheimer’s disease. “We actually see a population emerging of early-stage patients who can talk to you about their illness,” says Debra Cherry, executive vice president of the California Southland Chapter of the Alzheimer’s Association. Patients in their fifties or sixties with the early-onset form of the disease and who may be working in mentally demanding fields—say, accounting or law—find themselves inexplicably slipping. “It’s poignant,” says Cherry. “You have people who are so brilliant but can’t do the simple things.”
As the disease creeps toward its conclusion (the average time from diagnosis to death is eight years), patients are placed in nursing homes and hospices by exhausted spouses and children. They kick and bite and fling dinner trays. They shuffle up and down the halls after being put to bed. They see imaginary animals and accuse devoted caregivers of theft. They erupt in bouts of sobbing or laughing—an eerie phenomenon first described in medical literature by Charles Darwin and now known as pseudobulbar affect. Eventually they lose the ability to walk or swallow. “It’s all gone to shit,” a retired physician with advanced dementia said to me on a geriatric psychiatry ward during my final year of medical school. He no longer knew his name or recognized his wife, and he could feel the erosion of his mind, his personhood, the identity he’d spent his life developing.
The human brain, as philosophers like to point out, is the only thing in the universe that ponders itself. There is much to contemplate. Containing tens of billions of nerve cells, called neurons, which are networked by 100 trillion tiny junctions, or synapses, the brain is saddled with the hellish multitask of running the body—dispensing hormones, regulating heat and hunger, moving limbs, breathing, blinking—like the stage manager of a microscopic, never-ending Cirque du Soleil show. That’s only the side work. The brain’s magnum opus is generating consciousness, wherein the input from our senses converges with the din of our thoughts and the fog of our memories to produce the wispy realm known as the mind. So this hardworking brain of ours, as Emily Dickinson wrote, is not just wider than the sky; it is also deeper than the sea.
Alzheimer’s fills the sky with ash and the sea with six-pack rings. Between cells a sludgy protein, known as amyloid, permanently fouls synapses, while another protein, named tau, blocks the flow of nutrients in the neurons. As the dreck piles up, the synapses collapse and the neurons die; the shriveled areas at the temple and front of the brain are plainly apparent in the CT scans of late-stage Alzheimer’s patients. The illness tends to hit the left side of the brain harder, which is probably why patients often lose the sense of smell in their left nostril before their right one.
Having a way to deduce your genetic risk for Alzheimer’s would certainly be helpful (and some health insurance plans do pay for genetic testing if requested by a physician). Far more useful, however, would be a screening method that could detect the disease itself in its early stages, when those subtle lapses and gassy brain blunders are mistaken for normal aging but the neural deterioration is already well under way. “Some reports claim that once you have Alzheimer’s, you’ve already lost 50 percent of your brain cells,” says Keith Black, a neurosurgeon at Cedars-Sinai Medical Center.
Indeed, the origins of Alzheimer’s in an individual may go back decades—and may hinge on how well the brain was functioning before the trouble began. In a landmark study of 678 Roman Catholic nuns, nearly 80 percent of those who’d written weak, formlike autobiographical essays in a convent in their late teens or early twenties went on to develop the disease, versus only 10 percent of those who’d written more narrative essays. The difference may reflect what’s called cognitive reserve, which is the surplus capacity to reason and remember. It varies from person to person, and a brain with good cognitive reserve can compensate for the destruction wrought by Alzheimer’s, effectively zeroing out the disease, much longer than one with poor cognitive reserve.
Black, who is 56, started investigating new ways to detect Alzheimer’s several years ago after his mother was diagnosed with it. He homed in on a noninvasive method to spot amyloid buildup in the brain. Amyloid can be found using a scanning technology called positron emission tomography (PET), but it’s expensive, not widely available, and uses radiation, just like a CT scan. So Black teamed with researchers from Israel to hunt for amyloid in the retina—the complex, light-detecting layer at the back of the eye that is, neurologically speaking, an extension of the brain.
Previous investigators, finding no retinal amyloid, had dismissed the effort as a biochemical snipe hunt. The breakthrough came when curcumin—the active compound in the Indian spice turmeric—was found to bind to amyloid, rendering it visible on a specially configured optical scan that’s painless and uses no radiation. Black’s colleagues recently tested the new technology against a PET scanner on 40 people. “Everyone who was positive on the PET scan was also positive on our retinal imaging,” he says. “We didn’t miss anyone.” He anticipates receiving FDA approval by the end of this year and hopes eye doctors will start making the amyloid exam a standard test for all patients over 50 by 2019.
Far less likely to emerge anytime soon is a drug that can cure Alzheimer’s. Available drugs do little to slow the disease’s progress. Recent work has focused on preventing or removing amyloid plaques, but “so far, this has been a failure,” says Lon S. Schneider, a professor of psychiatry and director of the California Alzheimer’s Disease Center at USC. Scientists let out a collective groan when results came back in 2012 from a study showing that patients who took the experimental drug bapineuzumab didn’t improve, even though the drug succeeded in removing as much as 25 percent of the amyloid buildup from their brains. So Schneider and a colleague are working with allopregnanolone, a natural compound that can regenerate neural tissue in lab mice. Meanwhile others continue to look into curcumin. For instance, UCLA researchers have found that the compound can prevent amyloid accumulation as well as cognitive deficits.
For now, though, your best option to ward off Alzheimer’s is pretty simple: Keep your cholesterol and blood pressure in check, lose weight if necessary, and avoid cigarettes. Smoking, high blood pressure, high cholesterol, and obesity are all associated with a higher risk for dementia, of which Alzheimer’s is the most common cause. For that matter, air pollution has been shown to have links to cognitive deterioration as well.
Living in L.A., you may not have control over the air you breathe, but you do over the food you eat—and the less fat it contains, the better. Evidence is stronger still for exercise. Researchers in Finland recently found that Alzheimer’s patients who’d enrolled in a long-term exercise program slowed their rate of functional decline by more than half. Routine mental workouts can also help. “There is good evidence that many of the so-called brain exercises do improve brain function,” says Schneider. That’s part of the pitch by Web companies like Lumosity, which sells subscriptions to its service. Then again, Sudoku works, too. With puzzles in the paper and free online, you can do a little mental work calculating the money you saved.