SAG HARBOR
Fall 2014
There’s more we want to do, though, than bide our time at home. Almost every day, we get media requests for interviews with B. and me. We knew that B. was a national figure; we didn’t anticipate that her illness would stir such interest and concern across the country, so much that the story just keeps reverberating. Partly, it’s B. People feel they know her, and in a way they do: the still-warm, still-gracious woman they see on TV is B., and audiences can feel that glow as much as I do. Partly, it’s the families of those 5.2 million Americans who have Alzheimer’s, and the millions more of their friends and relatives. I believe they take comfort from B.’s courage in confronting this awful disease. At the same time, I think the audience is wider even than that. Let’s face it: we’re all terrified of getting this disease, and with every name or fact we forget, we feel a little stab of fear. Maybe we, too, we think, are destined to get Alzheimer’s.
I want to turn that fear into positive action, as we’ve done with ours.
Here’s my hit list so far:
B. and I want to do all we can to make people aware of Alzheimer’s early symptoms: those little signs of difference that so often get misinterpreted by families as marital tensions, or irascibility for no reason on the part of a parent or loved one. Knowing that those signs may denote Alzheimer’s isn’t terribly reassuring, but ultimately it’s better to know than not and it can make a difference to treatment.
The doctors can’t stress this enough: acting on those little signs instead of sweeping them under the rug is the best possible thing you can do. Fear keeps all too many of us from seeking medical help—and for those who do have Alzheimer’s, it only allows the symptoms to grow worse. The two existing classes of Alzheimer’s drugs are feeble, but to the extent they work, they seem to do so with patients who don’t yet have the disease, only its precursor symptoms.
This is a message we’ll be beating the drum about again and again and again. The PET screen for amyloid plaques is a hugely important new tool in the fight against Alzheimer’s. It’s not a treatment and it’s not a cure, but knowing for sure whether or not you have the disease—or, to be technical, whether you have the amyloid plaques associated with the disease—is a big step forward. For many who have Alzheimer’s-like symptoms, it may bring absolution: a plaque-free PET screen. In that case a patient can know those little signs of difference are just normal signs of aging. Howard got a call not long ago from the wife and children of an eighty-two-year-old chairman and CEO of some major company. The chairman was having his lapses, at home and at work, and had begun to plan for his retirement. Almost as an afterthought—sure, as he was, that he did have Alzheimer’s—the chairman got a PET imaging scan. He was amyloid-plaque free. With that, he could notify his board he’d be staying on another two or three years. Coincidence or not, he felt his memory sharpen overnight.
For those whose screens show these plaques, but not many as of yet, the test can be a wake-up call to start a lifestyle regimen—good diet and vigorous daily exercise—as well as the drugs. The cost of PET imaging is considerable—about five thousand dollars—and Medicare shows no sign of planning to cover it. Result: as many as 20–30 percent of Americans who would test positive for Alzheimer’s or some other form of dementia don’t get diagnosed. That’s why we’re supporting the Hope for Alzheimer’s Act, more fully called the Health Outcomes, Planning, and Education (HOPE) for Alzheimer’s Act. It calls for Medicare coverage not only of PET imaging but of care planning, both for the patient and caregiver.
To Howard Fillit, our doctor, an even more exciting development in screening is “imaging agents” that target the tangles—clumps of tau—that invariably appear with dying brain cells and may, as a result, be as good or better an indicator of Alzheimer’s than the amyloid plaque screen. Amyloid plaques, as Howard observes, can be present in individuals who never develop symptoms of Alzheimer’s—for reasons not yet known. The tangles, he feels, “are likely to be a better surrogate for tracking Alzheimer’s progression and determining the efficacy of any given drug.” These new imaging tools, he adds, “may work for related diseases that also have tangles, such as frontotemporal dementia, and could be used to assess tau pathology in the brain after a traumatic brain injury.”
We’ll continue stressing the importance of a healthy diet, and of vigorous, daily exercise. Just in the last couple of years, researchers have found proof that especially with early-stage patients, the right diet and exercise not only block progression of the disease but enlarge the brain, grow new cells, and turn on various genes and proteins that keep brain cells alive. Other so-called lifestyle factors include moderate (or no) alcohol consumption and management of hypertension, high cholesterol, and diabetes.
We want all Americans to be aware of Alzheimer’s symptoms, and to act on them if they appear. But we feel a special obligation to our fellow African Americans, given the shockingly higher incidence of Alzheimer’s in the black community. We know that type 2 diabetes runs rampant in the community, too, and that there appears to be some link between the two diseases. Is it a coincidence that both of B.’s parents, along with all her father’s siblings, and one of her three brothers, died of diabetes, and that B. then got early-onset Alzheimer’s? I think it’s all too likely that both of B.’s parents and her brother Gary, had they lived longer, might have gotten Alzheimer’s and died of it instead.
All over this country, but especially in the South, African Americans are struggling with both early- and late-onset Alzheimer’s, and not doing what they can do to save or prolong their lives. Not going to primary care doctors for candid talk about symptoms. Not getting PET imaging diagnoses. Not participating in clinical trials that can unlock the mystery of why twice as many African Americans as Caucasians get Alzheimer’s in the first place—and which drugs, at which dosages, may at last be able to treat or even cure the disease in the black community. Tuskegee remains a horrible stain on the federal government and the scientists who administered it. But it’s a long-ago time and place, and laws have been passed to keep it from happening ever again. Researchers have to tell you what they’re giving you, how it might help, and what its side effects might be. And they have to get your consent.
I’ll tell you this: I’m going out to help recruit participants for those trials. I can’t make new drugs and I don’t have the money to fund scientists to do it for me. But I do have a voice—a pretty loud one, I’m told—and I can use it to put out the word. It’s very simple: you’re either in one of those trials or you’re not. You’re part of the solution, or part of the problem.
Along this journey, I’ve learned to lower my expectations. I know some years may pass before a first generation of “disease-modifying” drugs—not just drugs that treat mild symptoms—gets to market and starts to change the story we know about Alzheimer’s and its stages. I know, most important, that the chances of seeing the fog lift from B.’s brain are very slim. Yet in recent months, as I’ve talked to experts and learned more about this disease, two names have come up again and again: two researchers racing down similar paths to a possible breakthrough after all. As it happens, they work a short walk away from each other, in the research complex of Massachusetts General Hospital, overlooking the Charles River in Boston.
The drugs they’re working with aren’t new, exactly. What’s new is their approach.
If they’re right—and a lot of their colleagues think they are—the key to Alzheimer’s may lie as much in when the right drug is given as in what it is.