"Is what I'm experiencing ordinary midlife forgetfulness? Or do these memory lapses signify something more serious—like the first signs of Alzheimer's disease?"

Practically every day, someone asks me these questions. And I wish I had better answers. One evening, a white-haired gentleman rose to his feet in a jam-packed auditorium. Anxiously, he asked me to confirm that forgetfulness was a perfectly normal part of aging, without pathological implications.

That, to my sorrow, I could not do. Reluctantly, I told him what I knew. Every day, a new study rolls out of a university lab confirming that Alzheimer's isn't a disease that suddenly rears its head in old age. Current research shows that decades before clinical symptoms arise—in middle age or even before—the seeds of Alzheimer's are already planted. To insist otherwise is to indulge in the most unhealthy sort of denial.

Like the rest of our bodies, our brains change as we get older. Proteins that were once smoothly soluble begin to aggregate, impeding communication between neurons, resulting in mild forgetfulness. For many of us, that's where it stops. But in others, those same tiny proteins get out of control, triggering the development of dense plaques and tangles that surround neurons, infiltrate them and eventually strangle them. Today's scientists are working hard to develop a test that will show—at the earliest possible moment—who’s taking the wrong fork in the road.

The goal of nearly every Alzheimer's researcher is to find a way to identify the beginning of the disease process. "If we can meet this disease in the earliest stage and counteract it with drugs that reverse the damage, science would no longer be in the position of needing to build new neurons," says John Q. Trojanowski, director of the Penn Institute on Aging and Alzheimer's Disease at the University of Pennsylvania. "It is in your forties, or maybe even younger, that normal memory loss begins to diverge from pathological memory loss. In my lab, we’re spending a lot of time trying to define that fork in the road, where you either continue to lose a little bit of your memory capacity each year, and remain essentially normal, or you take the other fork, where you are on a downward trajectory, culminating in dementia."

Trojanowski's lab at Penn is on the leading edge of the hunt for a biological marker—the equivalent of a pregnancy test—for Alzheimer’s disease. This "biomarker" must be fast, painless, inexpensive and able to pick up indicators of the disease at a very early stage, permitting early diagnosis, before neurons begin to die. In order to know whom to treat, it's essential to know who is vulnerable. As part of a National Institute of Aging investigation, the Alzheimer's Disease Neuroimaging Initiative, or ADNI, Trojanowski’s lab has made significant progress in tracking down a marker for the elevated presence of tau and amyloid beta proteins in cerebrospinal fluid. It's accurate, and meets most of the criteria, but is of limited use in a once-a-year doctor's check up, since not many of us would like to top off our annual physicals with a spinal tap.

That's why people got so excited earlier this week when scientists at Stanford University announced that they had developed a blood test that can diagnose Alzheimer's disease years before memory loss is evident. The test shows a 90 percent accuracy rate in its ability to predict who would develop Alzheimer's disease two to six years in the future, by measuring eighteen proteins involved in cell signaling. The proteins that neurologist Tony Wyss-Coray assessed were not even on the list of "promising" blood chemicals identified in 2003 by the National Institute on Aging study—but often, that's how science works. For years, researchers pursue a hypothesis, adding bit by bit to existing knowledge—only to have another team of researcher turn that hypothesis on its ear and shout "Eureka, we’ve found it!"

The Stanford blood test, promising as it is, requires more extensive testing, in a larger sample of patients and control subjects, including confirmation of accuracy that can emerge only after the autopsies of deceased study participants. It will take several years to do these studies, and in the meantime, given the intense focus on this effort, other biomarkers in blood and urine are likely to emerge. That's good news for all of us. Within a few years, when you go to see your primary care practitioner, there will be one more box checked on the sheet you take to the blood lab—one that will tell your physician what’s going on in your brain. "It goes painful step by painful step," John Trojanowski emailed me, when I asked him what he thought of the Stanford news, "but this is progress that takes us closer to meaningful therapies."

For more on biomarkers, go to Carved in Sand Chapter 1, Your Unreliable Brain, and Chapter 18, Do You Really Want to Know.

There’s no such thing as a quick fix—or is there?

I’ve spent much of the last five years researching vitamins and supplements that maximize cognitive ability. In brief, here’s what I know: In order to keep your marbles, you need plenty of antioxidants, essential fatty acids, B vitamins and magnesium in your diet. Unless you’re a grazing animal, it’s highly unlikely that you can obtain all the antioxidants you need exclusively from the food you eat. (You’d have to gobble fruits and veggies all day long, which can get messy in the car.) After you swallow as many antioxidants as you can (and don’t forget spices like curcumin—the yellow pigment found in turmeric—and cinnamon), you can supplement with coenzyme Q-10. It’s one of the few antioxidants that’s fat soluble, which means that it can rapidly cross the cell membrane, the better to protect you against free radicals.

About 40 percent of midlife Americans are deficient in essential fatty acids, also known as Omega-3s, which are critical for optimal neuronal function. EFAs comprise the raw material of myelin, the covering of lipid fat that surrounds a neuron’s delicate branches. They also form the cell membrane, which maintains a neuron’s structural integrity. EFAs make the membrane more fluid and flexible, allowing the cell to be more receptive to incoming signals. Top sources of EFAs are fatty coldwater fish like wild salmon, but you can also get EFAs from almonds, pecans, soybeans, walnuts, flaxseeds and avocado. Because of the danger of mercury toxicity, you can’t eat sufficient cold-water fish to satisfy your EFA requirement, but you can bolster your diet with supplements and get what you need: EFAs are available in mercury-safe “Omega-3” fish oil capsules.

Check your multivitamin to make sure that there are plenty of B-vitamins on board (and don’t expect to find enough in a cheap supermarket brand). Put your vitamin through the folate test—if the label lists 400 micrograms of folate, it’s likely to be a good one. B vitamins are required for the conversion of glucose to energy—and glucose is what fuels your brain.

Magnesium is the mineral du jour when it comes to maintaining your midlife cognitive chops. Up to 80 percent of people in the United States are magnesium deficient, a condition that may result in a short attention span, confusion, memory loss, insomnia, mood changes, apathy and fatigue. Sound familiar? Unless you’re a serious fan of Brussels sprouts and kale, there’s practically no magnesium in the food we eat. Research emerging from MIT shows that 420 milligrams of magnesium for males, and 320 milligrams for females helps maintain the plasticity of nerve cells, as well as several levels of neurotransmitters. Taking calcium and magnesium helps both supplements work better—and may contribute to sounder sleep.

Yesterday, I was paging through Science News, one of the scientific journals I read every week, and I found something that sent me scuttling to the Whole Foods vitamin and supplement aisle. It was an article about Rhodiola rosea, a sweet-smelling mountain herb that has been studied for decades in Russia. I'd heard about it before, but I'd put it on a long list of untested herbs of questionable value. (Virtually all studies that come out of the former USSR find whatever treatment is being tested to be effective. In the case of rhodiola, the details of research remained locked away because the herb was considered a top military secret.) Here, on the page, were the results of several high-quality clinical trials, in Sweden and the U.K., in conjunction with Russian investigations.

Apparently, the root of this yellow, flowering plant—one of a family of plants known as adaptogens—can do some remarkable things. Laboratory and animal studies show that the herb may inhibit cancer cells, protect healthy cells from toxins, and correct enzyme imbalances associated with diabetes. In animals, rhodiola lowers the stress hormone known as cortisol, and acts as an antioxidant. In addition, four trials with human volunteers show that rhodiola extracts can boost mental performance, prevent altitude sickness and reduce fatigue. It has been used successfully to alleviate depression. And it seems to help people who are suffering from the neurocognitive side affects of Lyme disease. In Russia, athletes and cosmonauts use it because it appears to increase aerobic capacity, speeds recovery of the circulatory system, and allows them to function under conditions of sleep deprivation, while maintaining their cognitive capacity.

How does it work? Russian studies suggest rhodiola optimizes serotonin and dopamine levels, and stimulates production of endorphins, but that’s obviously just the tip of the iceberg—more research is needed. If the herb can alleviate depression and improve mental functioning, it would be valuable indeed. Typically, antidepressants, which are strongly sedating, make patients a little foggier than they’d normally be.

A typical dosage is two 100-milligram capsules, taken in the morning. Taken too late in the day, rhodiola might interfere with sleep. There are no known safety issues with rhodiola, but comprehensive studies have not been performed. Check with your physician before taking it or any other vitamin or supplement, especially if you are taking other medications, including antidepressants. The response to this herb is very rapid—some people report improved mental states in a matter of days.

I’m swallowing my capsules right now. Give me a few weeks, and I’ll let you know. I’m not depressed. But it would be nice to feel a little sunnier as winter sets in. Hope springs eternal—maybe there is a quick fix after all.

For more on the subject of brain nutrition, take a look at “Swallow This,” Chapter Six of Carved In Sand: When Attention Fails and Memory Fades in Midlife.

I don’t usually send jokes over the Internet (or even tell them very often), mostly because I can’t remember them. This howler arrived last week from my cousin Jodi—who received it from a friend whose father was in the pharmaceutical business. I just had to pass it along. Take everything between the quotation marks with a grain of salt, please…

"In the field of pharmacology, all drugs have two names, a trade name and a generic name. For example, the popular drug known by the trade name of Tylenol also has a generic name of acetaminophen. Aleve is also called naproxen. Amoxil’s generic is amoxicillin and Advil is called ibuprofen.

The FDA has been looking for a generic name for Viagra. After careful consideration by a team of government experts, it recently announced that it has settled on the generic name of Mycoxafloppin. Also considered were Mycoxafailin, Mydixadrupin, Mydixarizin, Dixafix, and of course, Ibepokin.

 Pfizer Corp., which manufactures Viagra and is searching for new formulations that will allow the company to maintain its market share, announced today that Viagra will soon be available in liquid form, and will be marketed by Pepsi Cola as a power beverage suitable for use as a mixer. It will now be possible for a man to literally pour himself a stiff one. Obviously we can no longer call this a soft drink, and it gives new meaning to the names of "cocktails", "highballs" and just a good old-fashioned "stiff drink." Pepsi will market the new concoction by the name of 'MOUNT & DO'."

Guffaw, definitely. But a thought for the day:

Right now, more money is being spent on developing and marketing erectile dysfunction drugs ($2 billion in 2006) than the federal government is committing to Alzheimer's research—around $1 billion. You know the statistics all too well: Five million Americans have Alzheimer's disease, including 500,000 people under the age of 65. Earlier this year, the Alzheimer's Association estimated that someone in America is diagnosed with Alzheimer’s every 72 seconds. It's the seventh leading cause of death in the United States and nearly as prevalent in Japan and Europe. The direct and indirect costs of Alzheimer's in the U.S. amount to $148 billion annually. In 2005, state and federal Medicaid spending for nursing home and home care for people with Alzheimer's and other dementias was estimated at $21 billion; that number is expected to increase to $27 billion by 2015. If the disease proceeds unimpeded, by 2030, the number of people with Alzheimer's is projected to increase to 7.7 million. When you consider that by 2030, almost one in five Americans will be over sixty-five, it's apparent that we face a health burden that will swamp us.

If you don’t want to end your life this way, you need to let Washington know about it. How fast we can get this disease under control depends largely on how much money we can throw at it. New tools that will permit early diagnosis and treatment are on the horizon, including biomarkers that assess protein levels in urine, cerebrospinal fluid and blood. There are currently eight drugs in Phase III clinical trials for Alzheimer's. One primary prevention trial costs more than $30 million and takes five to ten years. So write to your representatives in Congress and tell them you want a treatment sooner, rather than later. Even better, sign up at your local university Alzheimer's center to participate in a research—they need normal subjects as well as subjects who may be in the early stages of dementia. For more information about participating in clinical trials, visit the Alzheimer's Association website. For a list of universities with active Alzheimer's research programs, go to this list on my website. For more on the subject of Alzheimer's research, see Chapters 17 and 18 of Carved in Sand: When Attention Fails and Memory Fades in Midlife. You’ll be doing yourself—and the rest of us—a big favor.

I don’t mean to be unsympathetic, but I have to believe that from the day he signed his contract with the New England Patriots, middle linebacker Ted Johnson knew he had chosen a career path that mandated headlong collisions with speeding flesh dressed in helmets and shoulder pads. The same could be said for other professional athletes whose brains have made the news in the last year—the late Andre Waters, formerly of the Philadelphia Eagles, and Bob Brudzinski, who played 13 seasons with the Miami Dolphins and the Los Angeles Rams. They took some hard knocks—okay, a lot of them—and they've paid a grave price.

But what about the rest of us? You don’t have to be a pro football player to put your head in jeopardy. According to the National Center for Injury Prevention and Control, at least 1.1 million people each year sustain mild traumatic brain injuries. No doubt, that number is set too low: Most people who sustain such "minor" injuries do not go to the emergency room or a doctor’s office. They go home and lie down on the sofa.

The assumption has always been that our skulls—which seem pretty hard—function as protective shells. In fact, what’s inside—a brain with the consistency of gently scrambled eggs—is very vulnerable. Throughout our lives, the injuries that we experience accumulate in a way that can result in noticeable cognitive deficits. It is impossible to say how many middle-aged adults who presume they are suffering from age-related memory impairment, or maybe adult ADHD, are actually feeling the consequences of a series of earlier head injuries.

Until a decade ago, scientists regarded mild traumatic brain injury—where there is no loss of consciousness or evident structural damage—as inconsequential. You were expected to recover quickly and entirely from such an accident, and anyone who presented symptoms after a month or two was considered to be "malingering," probably in the interest in settling a large lawsuit.

Only in the last several years have experts begun to understand what happens when your brain meets the bony protuberances behind the forehead, surrounding the prefrontal cortex. Forget about being knocked unconscious: Most mildly concussed individuals remain wide awake, working their way through a variety of symptoms, from feeling dazed and confused to seeing stars. Often, there's a touch of amnesia involved—they're not sure what happened to them, before, during or immediately after the impact.

As used here, the word "impact" requires some clarification. You can have a concussion when your head encounters an immovable object—for instance, the windshield during an auto accident. But the collision can also occur internally. Slam on the brakes when you’re driving twenty miles an hour, secure in your seatbelt and guess what: Your car screeches to a stop, but your brain keeps going forward. In fact, this three-pound bolus of fat smacks your bony prefrontal protuberances at your previous pace, and then begins to imitate a Superball, ricocheting all over the place inside your skull.

Car accidents are responsible for the bulk of mild traumatic brain injuries, but increasingly, we're finding other ways to mess up our heads. Sports injuries account for more than 20 percent of the mild traumatic brain injuries each year. You can have a closetful of helmets—biking, riding, rafting, hockey, lacrosse, skiing, even river rafting—and while they'll do wonders to preserve the exterior of your skull, they don’t help much with what is inside. You can wallop your head executing perfectly innocent maneuvers: one Los Angeles woman I know walked headlong into a low hanging branch of a sturdy oak tree while reading a catalog from an art gallery she'd just visited, and knocked herself flat. Some weeks later, she was cleaning up a Coke that had exploded in the little refrigerator under a granite counter in her family room. She stood up suddenly—and wham, she was down again.

Right about the time that you’re catching your breath, impressed with your evasive driving skills and your anti-lock brakes, the cascade of damage inside your head begins. Researchers are still trying to understand exactly what happens when these injuries occur. One common hypothesis is that arteries in the brain constrict, make it impossible to deliver sufficient glucose, but that is only part of the story. When the brain makes contact with the sharp bones inside the skull, small blood vessels may rupture, releasing blood into the cranium, which, unlike other parts of the body, cannot expand to encompass it. The brain is uncomfortably squeezed for space. "Second impact syndrome," as too often experienced by Mr. Johnson and other athletes, is especially dangerous because that second hit increases that intracranial pressure. Often, as the brain does its Superball routine, microscopic tears develop in the myelin sheath surrounding the nerve fibers that transmit information from one part of the brain to another. These torn nerve fibers, called axons, develop scar tissue, which will eventually affect the speed and efficiency of synaptic impulses.

Typically, we put our mild head injuries behind us, heading back to work or school. Weeks or months later, we’re befuddled when we find that we’re suffering from inexplicable impairment—typically, problems with working memory and executive function, cognitive faculties regulated mostly by the prefrontal cortex. The real damage shows up long after the injury has been forgotten, as ruptured axons, rife with scar tissue, begin to die, reducing the capacity to process information. For many people who experience mild traumatic head injuries, the senior moments start coming fast and furiously, no matter what age they are.

It’s becoming evident that even mild traumatic head injuries (defined as injuries where you do not lose consciousness) may lead to an increased risk of Alzheimer's disease, particularly if you are a carrier of a genetic variant called the ApoE-4 allele. So far, most of the research (performed on rats at the University of Pennsylvania's Head Injury Center) suggests that repetitive mild brain trauma accelerates the emergence of Alzheimer's disease. No one has nailed down how this happens, but the theory is that the axons sheared in the Superball routine release a sudden bounty of lipids, which attract hordes of greedy free radicals, which in turn step up oxidative damage to the brain. It's been hypothesized that excessive oxidation makes neurons more vulnerable to the effects of amyloid proteins, and may also escalate the development of amyloid plaques, which slowly strangle nerve cells.

In a recent edition of the New York Times, journalist Alan Schwarz wrote an excellent piece about how head injuries are affecting 1.2 million teenagers who play high school football. As I said earlier, I'm not overwhelmed with sympathy for pro players, but my heart goes out to these high school kids. They're suffering from a common adolescent misconception: Their fervent belief in their own immortality. They keep their head injuries secret, conscientiously reporting, after they've been hit, that they feel fine—not the slightest hint of headache, no nausea or disorientation, in order to remain in the game. Pre-season, team members submit to baseline neuropsych evaluations, but they've figured out how to work 'em. Intentionally, they perform poorly—so that if they're hit, and experience cognitive sequellae, there won’t appear to be a change in their performance. Very tricky—but in large numbers, they make themselves vulnerable to second-impact syndrome.

These high school players are also suffering from lack of information—in his article, Schwarz noted that most players "did not quite know what a concussion was," and still believed that to have suffered one, you had to fall unconscious. Teenagers, observes Schwarz, are "more susceptible to immediate harm from such injuries because, studies show, their brain tissue is less developed than adults’ and more easily damaged. High school players also receive less capable medical care, or none at all." According to Schwarz, many parents and coaches exacerbate the situation by encouraging players who have taken a hit to get back in the game. One source reported that "he’d seen coaches...berate and ostracize players who complained of concussive symptoms." Parents have been known to "shop a doc," who is willing to give a concussed teen player a clean bill of health, another coach told Schwarz, so that their child can return to the game.

At least 50 high school or younger football players in more than 20 states since 1997 have been killed or have sustained serious head injuries on the field, according to the New York Times' research. The dedicated and sometimes obsessively competitive people who coach children's sports ought to acknowledge that they are not capable, at a glance, of assessing whether a young athlete might have suffered a concussion. No matter how good a player is, the only place for him or her after a bell-ringing incident (even a suspected one) is on the bench for a couple of weeks, to avoid the vastly increased danger of second-impact syndrome. Parents should demand this, but unaware of the consequences, most do not. They want to see Junior back in the game. Maybe, if he gets a little more play, he can make it to the NFL.

People ask me all the time why they blank on names. One scientist, Marilyn Albert, the director of cognitive neuroscience at Johns Hopkins, told me that the failure to retrieve people’s names is so common that when her researchers select midlife or older subjects to participate in investigations of memory, they don’t count difficulty with names as an indication of emerging pathology. It’s just…well, normal.

That doesn’t make it a shred less irritating when you see your boss’s wife approaching at a rapid clip, and for the life of you, you can’t think of her name. Your eyes roll back in your head as you struggle for a hint. It’s Mary-something, but what? Anne? Lou? Jane? Beth? “Mary-hmmmm” you murmur as you greet her, hoping she doesn’t notice. (She does.) The rest of her name shows up in the middle of the night, wrenching you out of your dreams. It was in there, obviously—but where?

The trouble’s not new—Roman aristocrats always traveled with an alert slave called a “nomenclatur,” whose duty it was to supply his master with the names of acquaintances as they were encountered. I understand that while raising funds for campaigns, many of today’s political figures rely on a backfield of aids whose job it is to stand by and produce names as required, subtly thumbing the contact databases in their Blackberries. Great idea, but for most of us, not feasible—we’re working without a net.

After a great deal of research, I’ve concluded that the problem with modern names is that they fail to provide helpful clues that would allow us to fully encode the incoming data. The name “Ann” is lovely, but it does not come with recognizable characteristics—nothing about your neighbor is particularly Ann-like. There were some periods in history when it was de rigueur to insert a bunch of identifying information into a name. You were Jacob, son of Isaac and Rebecca, or Pocahontas, whose name translates as “always playful,” or, in early feudal Europe, The Lord of Something Really Big. When surnames came along—so the census takers for the Domesday Book could keep track—identifying names were handed out based on occupations—Smith, Baker, Weaver, Carpenter, Taylor, Brewer, Mason—or geography—Brook, Dale, Hill—or physical characteristics—Stout, Moody, Wise, Rich, Poor, Strong.

It’s rare to find anyone today whose given name or surname name reflects his or her demeanor, physique, hometown or profession. When you find one—the aptly named dentist, Dr. Needleman, comes to mind—you don’t have any trouble looking him up your address book. Given names or nicknames that allude to physical or psychological traits used to be good for a fond chuckle—I knew a hefty bartender everyone called Chubby, someone’s aunt who was actually named Pussy, my mother’s lively English friend who has struggled for years with the old-fashioned name Gay, and the trash collector of my childhood, who answered to Stinky. Understandably, these names are out of fashion, deemed politically incorrect. Still, I’d just love it if my electrician were named Sparky. I might not have to go through my entire database, searching for likely names, before I phoned him.

Although I do not know the name of a single human being in our local dog park, I can reliably greet most of the canine regulars. So many are endowed with names that mirror their physical traits or provenance. There’s Fidel, the Havanese, whose handle reflects his Cuban roots. There’s Einstein, a charmingly disheveled Schnauzer, and Bounce, a Jack Russell mix who came from the pound equipped with heavy-duty rocket thrusters. There’s Speed Bump, a Bassett-Beagle cross, and of course my dog Radar, who never leaves my side. My other pet, Rosie, a shepherd mutt, is more obscurely named, but I rescued her from the Santa Rosa Animal Shelter, a fact that allows people who make the connection to recall her name with ease.

Some well-known memory trainers (the kind who write books that promise that you can learn the names of thirty people at your next cocktail party) suggest that whenever you meet someone new, you ought to make a quick survey of his or her physical appearance—an attractive scarf on a redhead named Rose Sharf, for instance—and then try to link specific characteristics to the person’s name. Unlike dogs, people change things up, so this technique is loaded with ways to go astray. While you’re busily creating this image, you’re likely to miss the next six things that are happening, including introductions to several other people. It’s a fair bet that Rose won’t be wearing that pink scarf the next time you see her, or even twenty minutes later, if the day is warm. In fact, the next time you and Rose rendezvous, she may have decided that with her coloring, the russet tones are just too harsh—and gone blond.

What can you do? Before you go to an event where you are likely to see people you feel you should know, but haven’t encountered recently or frequently, review the list of names of those who will probably attend. Use a school or club directory, or check back through related correspondence. Email announcements or invitations, or anything that comes through the party invitation website Evite can be great memory joggers: Often the list of everyone who is invited is right there, in the “To” box, awaiting your inspection. Ignore it at your peril.

For more about how to stop forgetting proper nouns and other words, see Chapter Four in Carved In Sand, “Blocking, Blanking and Begging For Mercy.”

Phew! I’ve just returned from the San Rafael farmers’ market—gorgeous day here, so unusual for August in coastal northern California, where it’s typically foggy until noon. My kitchen counter is strewn with corn and tomatoes, peaches and nectarines, bags of salad greens, cartons of raspberries and blackberries, a huge bunch of sunflowers, a couple of fresh loaves of bread and a big hunk of creamy local blue cheese. Oh, yeah—there are two roasted chickens with potatoes, the delectable scent of which has, just short of noon, lured my sleepy thirteen-year-old son out of bed. Hands off, I tell him—those chickens are earmarked for dinner. I stood in line for twenty minutes for those chickens, chatting with two dozen other eager people, watching the birds go around and around, getting crispier and browner, on six spits engineered into the side panel of a vending truck. Now, I’m enjoying my just reward: a glass of fresh lemonade from a half-gallon jug, and time to write to you.

Before I get around to unpacking and washing all that produce, I wanted to record a few thoughts on the subject of brain fitness. A couple of weeks ago, I was supposed to be on a television show where—I learned at the last minute—I was to smilingly endorse the concept of computer software that helps keep your brain in shape. This, I know, is turning into a big business—venture capitalists are funding companies that bring these products to market, and TV shows, hungry for Boomer stories, are making much of these exercises. Go online and Google “brain fitness” and you’ll be inundated with new ways to sit in the dark, in isolation, in front of your computer screen, living your virtual life. Such programs have their place, of course—they can be very helpful to people who because of physical limitations are unable to get out and get their brain exercise in the real world.

I couldn’t bring myself to endorse such activities because I believe that a superior source of brain fitness exists right outside your front door.

If you’ve got two good legs (or for that matter, a nimble set of wheels), some grocery money, a sturdy tote bag or rolling cart and the gift of gab, I say leave the computer all alone in the dark, and get the heck out. Go to the farmers’ market early in the morning, just about the time the sun hits the peaches, and sop up the smells, colors and flavors. First stop: the baked-goods and coffee stand, where someone will hand you a dark brew topped with foam and a fresh-baked, slightly greasy chocolate croissant. Pause for a moment to savor these—bitter chocolate on the back of your tongue—then observe the families with flocks of giggling small children stuffing samples of juicy nectarines into open bird mouths.

When you’ve licked the crumbs from your fingers, pull a beautiful sun-warmed tomato out of the pile, squeeze it gently and sniff. If you don’t smell the vine and the soil in which it was grown, put it back and try another. No one will mind: This isn’t the supermarket, where nothing (not even the fish) is supposed to smell, everything is encased in plastic, and someone may stare if you hold a cantaloupe to your nose and sniff for signs that this ever grew from the ground. Chat with the woman responsible for growing and selling those farmers’ market tomatoes. She’ll fill you in on the crazily striped heirloom you’re holding in your hand. She may even nudge you in the direction of some other tomato—something a little sweeter, perhaps.

Maybe later, after you’ve made it home and had your lemonade (and a Sunday afternoon nap) you’ll share the bounty with friends. We’re having a couple over for dinner tonight. It won’t be fancy, just fresh greens—the kind you can’t find in the supermarket because already they’ve traveled a week to get there—and some tiny sweet peaches, sliced in two, and blue cheese, tossed in a light vinaigrette, with sugared pecans layered on top. Sweet, sour, tart, and perfect with that roasted chicken, potatoes and fresh bread—unless of course my kids get to those chickens first.

Don’t be surprised if you feel especially alert and alive when you pile your produce into your fresh basil-scented, yeasty car and head home. You’ve given your neurons a sensory treat—all five of them, sight, hearing, taste, smell and touch—the kind of workout they rarely receive. You’ve done your brain another favor—you’ve interacted with quite a few other human beings, breaking a pattern of social isolation that can become habitual with age. And, if you’ve followed my advice and invited your neighbor over to feast on the bounty, you’ve made a perfect score: Now, you’re going to have to exercise both your working memory and your long-term memory in order to make that blackberry crisp and bring it to the table perfectly browned and steaming hot.

For more on brain fitness, see Chapter Seven of my book, Carved In Sand: When Attention Fails and Memory Fades in Midlife.

“But that’s complete nonsense,” I muttered to myself, irritating the people sitting next to me in the theater. At the end of a long book tour, I’d taken myself to see Away From Her, a film from the talented young screenwriter and director, Sarah Polley. The movie addresses the relationship of Grant and Fiona Andersson, as they confront Fiona’s descent into Alzheimer’s disease. For me, it was a busman’s holiday: Several chapters of new book, Carved In Sand: When Attention Fails and Memory Fades in Midlife, address new options for early assessment, diagnosis and treatment of Alzheimer’s. There is still no cure, but caught very early in its trajectory, this disease can be treated and its insidious progress can be slowed. In the next five years, someone is going to find an answer.

To be fair, I might have been the only person in the audience – maybe in the film-going world – who had a problem with this picture. The critics reveled in the youthful Ms. Polley’s sensitive direction of her own script, based on Alice Munro’s short story, The Bear Came Over the Mountain. Julie Christie, always so beautiful, this time seemed illuminated from within, in a performance that would surely put her on the short list for an Oscar. Everything in the film gleams: the snow-covered Canadian lake where Grant and Fiona cross-country ski from their perfect cottage, the winter light through dark, lacy branches of trees.

Why, then, was I so bothered by what I saw? I knew there were people in this movie theater – in theaters across the country and ultimately around the world – who would go home, awash in silent misery, having recognized that they, or someone they knew, were already on the road to Alzheimer’s disease. They’d follow Grant and Fiona’s lead, and as a result, they’d make some terrible choices.

In the first few minutes of the film, we understand that for some time, both husband and wife have been aware of changes in Fiona’s memory. Youthful, energetic Fiona, who looks to be younger than 65, (although the film’s Web site notes that she’s meant to be 70) has been struggling for a while. Neither spouse has taken steps: Their attitude is one of quiet resignation. The Anderssons regard Fiona’s increasing forgetfulness with vague curiosity: How will it manifest itself next? Will she stow the frying pan in the refrigerator?

When Fiona skis out across the lake at dusk, and fails to return, Grant finds her asleep in the snow, and only then takes her to see the family physician. What happens in that office does not speak too highly for Canadian socialized medicine, but what usually occurs here in the States is much the same. The doctor, whose waiting room is full of mothers and children, administers a brief neurocognitive evaluation, through which Fiona stumbles, and promptly gives the couple the bad news: Dementia has Fiona in its grip.

In no time at all, the papers are signed, and Fiona – at her own insistence, and clearly against Grant’s wishes – is ensconced in Meadowlake, an assisted living facility that permits patients to remain on the lively first floor as long as they can feed and dress themselves, but sends them “upstairs,” where the bedspreads do not have cheerful flowers, when things get really bad. We never understand why Fiona is so determined to leave the home she loves, but she is: There is never talk of hiring a part-time home care aid. Not that she needs one: Fiona is so fully functioning that she packs her own suitcase, styles her magnificent silver-blond hair and leaves the house looking like she’s going to Le Cirque for lunch. One month after she arrives at this facility, she no longer recognizes her husband. She’s taken up with another man. Within the confines of that same cold, dark winter, she declines so much that she is moved to the dreaded “upstairs,” where she curls herself into a fetal position and prepares to leave the world behind for good. That makes for a great plot twist, but once again, it’s wrong: Early stage Alzheimer’s patients do not deteriorate that rapidly. Only in the last, brutal stages of the disease do patients fail to recognize their closest loved ones. The process of dying takes many years. In reality, Fiona, fit as can be from all that skiing, would likely live a decade or more at Meadowlake, no doubt swamping the family finances.

Maybe I was being unfair. I couldn’t blame Sarah Polley or Alice Munro for dispensing inaccurate scientific information, not when the emotional content of the film and the short story were so bang-on. I couldn’t blame Julie Christie for looking preternaturally young -- she is in fact 66 years old. Nor did I hold other movies to similar standards: After seeing last year’s hit, Little Miss Sunshine, I did not worry that everyone would go home, intent on reconfiguring their households to be equally dysfunctional. But Away From Her isn’t hyperbolic black comedy. It presents such an accurate portrait of the last days of a long marriage that I fear that people will accept it as gospel. If they do, they will not find their way to the right doctors. They will not go after this disease with all guns blazing. And increasingly – as scientists find new ways to intervene – that would be a mistake.

If you think that you or a loved one, or a colleague is experiencing significant or progressive changes in memory, it’s time to get a baseline neurocognitive evaluation. At the very least, this will allow for a straightforward assessment of change, six months later. Alzheimer’s disease can be treated aggressively, but you have to start early: Wait, like most people do, until destructive beta amyloid and tau proteins have woven themselves into the plaques and tangles that murder neurons, and there is nothing to be done. Never rely exclusively on a family physician for diagnosis: Instead of waiting months (or was it years?) to take their big truck down the road to Meadowlake, the Anderssons ought to have driven to the University of Toronto, or to McGill, where Fiona might have been evaluated by those who actually have expertise in diagnosing and treating memory disorders. (A complete list of Alzheimer’s research centers can be found on my website, at www.carvedinsand.com/ramin-links.htm. A list of experimental clinical trials can be found at www.clinicaltrials.gov. On that site, you’ll find trials of every piece of heavy artillery in the fight against Alzheimer’s – new drugs, vaccines, and gene-based therapy, shunts that sift the rogue proteins out of the bloodstream. At this moment, 153 such trials are recruiting participants. Over the next five years, one (or more) of them is likely to stop Alzheimer’s in its tracks. They are as varied as science is, but all rely on the willingness of human participants to volunteer. There is no need to sit quietly, like Fiona, and wait to succumb.

Cathryn Jakobson Ramin is the author of Carved in Sand: When Attention Fails and Memory Fades in Midlife, published by HarperCollins.