Inside the Dementia Epidemic: A Daughter's Memoir (35 page)

PET Scans

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ccording to Dr. Frank Longo, a Stanford University neuroscientist, two kinds of PET scans can be used to find evidence of probable Alzheimer’s disease in the brain, although each is imperfect. The first can show decreased levels of metabolic activity, but it’s not accurate enough to use for diagnosis. The second is an amyloid PET scan, in which an intravenous injection of florbetapir, a radioactive drug approved by the Food and Drug Administration in April 2012, binds to amyloid plaques. Amyloid PET scans show plaques on 96% of people with severe Alzheimer’s disease and two-thirds of those with mild cognitive impairment. Longo says this tool may be available to primary care doctors by the summer
of 2012, but it’s unlikely to be covered by Medicare at first. And he cautions that one-third of people aged 65 and over exhibiting normal cognition also show amyloid plaques on these PET scans—and they may never develop Alzheimer’s disease. The Alzheimer’s Association reserves judgment on this new tool, since “a positive scan...has limited utility at this point. Having amyloid buildup in your brain does not mean for certain that you have Alzheimer’s disease.” They recommend further research into the use of such PET imaging.

Spinal Fluid Tests

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spinal fluid test has been approved for use that identifies the presence of certain markers of Alzheimer’s disease—the proteins beta amyloid and tau—but it cannot accurately predict who will develop Alzheimer’s disease. Research on this spinal test showed that among the test subjects with Alzheimer’s disease, a huge percentage—ninety percent—had high levels of these proteins in their spinal fluid, but among those with mild cognitive impairment, only seventy-two percent had the markers. However, thirty-six percent of those with no symptoms of dementia still had the markers. If we want to test people before they develop symptoms of the disease, or to catch the disease early, the spinal fluid test is not accurate enough to be definitive. Many doctors and researchers are reluctant to recommend this test as it cannot confirm a diagnosis, and no treatments exist.

Biomarkers

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n May of 2011, an international workgroup of more than forty top Alzheimer’s researchers, organized by the Alzheimer’s Association and the National Institute on Aging (NIA) of the National Institutes of Health, published new criteria and guidelines for the diagnosis of Alzheimer’s disease—the first time the criteria and guidelines had been updated in 27 years. To make such a diagnosis,
they argue, it’s not enough to rely simply on observing a person’s behavior or to conduct a neuropsychological exam. Alzheimer’s research must find specific biochemical substances in the body that mark the presence or absence of the disease or that reveal the risk of developing the disease (“biomarkers”). Research must prove the value of those biomarkers, and it must assure the medical community that all diagnostic tests using those biomarkers will offer reliable results and remain consistent from one laboratory to another. That’s a tall order, and the committee acknowledges that it may take ten years or more for scientists to identify the correct biomarkers.

For now, the workgroup calls for intensive research on two types of biomarkers: the level of beta-amyloid in the brain, and damage or degeneration of nerve cells. Beta amyloid blocks the transmission of nerve impulses, and many researchers now agree that smaller beta amyloid particles, if not the larger plaques themselves, play a major role in the development of Alzheimer’s disease.

These smaller bits of amyloid beta build up in the brain years before plaques are formed or a patient receives a diagnosis of Alzheimer’s disease, and slowly kill the brain. Tests on mice show that the substance that eventually turns into amyloid plaques—amyloid precursor protein, or APP—causes the death of olfactory nerve cells, which are closely related to brain cells. (Loss of the sense of smell is one symptom of Alzheimer’s disease.) This degeneration starts not on the outside of the cells with larger plaques, as previously assumed, but inside the cells with this smaller amyloid substance. Dr. Jack Diamond, the scientific director at the Alzheimer Society of Canada, says that “by the time the plaques are formed, all the damage to the nerve cells has been done. A successful treatment would have to affect the amyloid molecules, not the plaques themselves.”

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Re-defining the Stages of Alzheimer’s Disease

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he international workgroup mentioned above also recommends that the stages of Alzheimer’s be revised to include the many years—perhaps decades—before any symptoms occur. They call this lengthy stage “preclinical Alzheimer’s disease.” When I read this, I find it frightening to think that Alzheimer’s could be stalking my own brain right this moment, while I am in my forties. Researchers and doctors cannot say for sure what is normal aging and what is preclinical Alzheimer’s disease. I already know that I am high-risk, with a mother who has dementia and shows so many symptoms of Alzheimer’s. The international workgroup calls for more research into the biomarkers of this first stage, to help us recognize, diagnose, and treat it before any decline occurs.

I
hope that in ten years the pages I’m writing here on Alzheimer’s research will be obsolete, that we will know how to prevent, treat, and cure Alzheimer’s disease and other dementias. For the moment, though, I continue to discover in my reading more promising—if sometimes conflicting—trends in Alzheimer’s research. As Diamond points out, “We’re now at a crossroads....Some of the things that we always assumed are now no longer acceptable as fully explaining the disease.”

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wo types of prescription medications have been approved by the FDA to treat the symptoms of Alzheimer’s disease. They are not a cure, and while they may lessen the symptoms of the disease, they will not slow its progression.

As enzyme blockers, the first group—the cholinesterase inhibitors—work by restoring the balance of neurotransmitters in the brain. They include Aricept (donepezil HCl), approved by the FDA in 1993; Exelon (rivastigmine), approved in 1997; and Razadyne (galantamine), approved in 2001. Exelon and Razadyne are approved for mild to moderate dementia, and Aricept is approved for mild to severe dementia.

The second type of medication is an N-methyl D-aspartate (NMDA) antagonist. Namenda (memantine), approved in 2003, can delay progression of some symptoms in moderate to severe cases of Alzheimer’s disease. It regulates glutamate, an important brain chemical.

There is evidence that a combination of these two types of medications—Namenda plus a cholinesterase inhibitor—is more effective at relieving the symptoms of Alzheimer’s disease than treatment with only one type. A two-and-a-half-year study by the Memory Disorder Unit at Massachusetts General Hospital, published in 2008, showed that test subjects with mild dementia who took a combination of these drugs experienced a slower decline
in memory and function than test subjects who took one type of medication or a placebo. A study published in the
Journal of the American Medical Association
in 2004 showed similar results with patients with moderate to severe dementia; when those already taking a cholinesterase inhibitor added Namenda, they experienced more of an increase in cognitive function and ability to perform activities of daily living than those solely on a cholinesterase inhibitor. Those on combination therapy also experienced a lower rate of side effects, especially gastrointestinal issues.

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s a large French multi-center task force states in their report,
Prevention of Progression to Dementia in the Elderly
, “our present state of knowledge is inadequate.”

None of us know if the health dictates we follow to avoid dementia will turn out in thirty years to have been bad advice. Mom taught me, for example, to avoid butter, to buy margarine because it didn’t have cholesterol (and because it was cheaper), but now the public knows about trans fat, and I wonder if that margarine and all the store-bought cookies she ate loaded her arteries with trans fat and contributed to her small strokes and dementia. (A 2011 study published by the journal
Neurology
shows a strong correlation between trans fat in the bloodstream and decreased brain function.)

Most scientists agree, however, that there are certain risk factors for Alzheimer’s disease. They include old age; a family history; serious head trauma; poor cardiovascular health; high blood pressure; stroke; diabetes; high cholesterol; obesity in middle age; a low education level (which predisposes someone to less learning and brain development over their lifetime); and smoking.

Exercise

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ome researchers say that exercise may be our most powerful antidote for Alzheimer’s disease. Because aerobic exercise increases blood flow to the brain, stimulates the growth of new brain cells,
and decreases the risk of heart attack, stroke, and diabetes, the Alzheimer’s Association recommends thirty minutes of daily exercise.

A recent study by neurologists at Rush University Medical Center shows that daily activity of all kinds—from formal exercise to activities such as washing dishes, cleaning, and cooking—may reduce the risk of developing Alzheimer’s disease, even in people over age 80. In another study, subjects who walked forty minutes a day for a year regained volume in their hippocampus, reversing brain shrinkage. In a third study, people with mild cognitive impairment who did resistance weight training two times a week over six months showed an increase in their memory and executive function (the ability to multi-task).

Mental Stimulation

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ocial activity and mental stimulation are also crucial. Combining social activity and mental stimulation with regular exercise is more effective than doing only one or the other. Sports, cultural activities, emotional support, and close personal relationships are all key. We should work as long as we can, volunteer, join social clubs, and travel. We should turn off the television, read, write, do crosswords and puzzles. Play games, do memory exercises, learn a new language, or learn to play an instrument. In fact, if we challenge ourselves regularly, our brains will continue to create new cells and connections.

In the last ten years Mom lived at the cottage, she had little social interaction, scant mental stimulation beyond reading, and no exercise beyond climbing the hill to her car once or twice a week in winter.

My life in an intentional community is quite different. I can hike with a friend through our fields, work with a team to cook a village meal, or play an instrument and perform skits in our village
talent shows. There’s always something to do, and someone to do it with.

The Role of Diet

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he Alzheimer’s Association recommends a low-fat, low-cholesterol diet, but acknowledges that all cholesterol is not the same: research suggests that HDL, or “good” cholesterol, may help protect brain cells. They recommend lots of dark vegetables and fruits that are high in antioxidants; mono- or polyunsaturated fats such as olive oil, cold water fish high in Omega 3’s (salmon, tuna, mackerel); and nuts such as almonds, pecans, and walnuts. Vitamin E, or vitamin E and C together, vitamin B12, and folate may also decrease the risk of Alzheimer’s.

In 2005, when Mom lived with us, I barely had time to think of my own health. Not only was I seriously overweight, but I was insulin resistant and pre-diabetic and didn’t know it yet. (Insulin in the blood delivers glucose—blood sugar—to the body’s cells. With insulin resistance and pre-diabetes, cells grow resistant to the insulin, too much glucose remains in the blood and damages organs, and then the pancreas pumps out even more insulin to force the cells to absorb the glucose. If the pancreas grows exhausted and stops producing enough insulin, you get Type II diabetes.) I had also become quite allergic for the first time in my life to pollen, dust, and wheat, and was prone to frequent attacks of bronchitis.

Gradually, over the past few years, while a variety of facilities have taken on the care of Mom’s daily physical needs, I have paid more attention to my own. I’ve lost weight and lowered my blood sugar level on a low-carbohydrate, wheat-free, sugar-free diet under the supervision of a nutritionist. I get shots every two weeks for my allergies, and garden, walk, and swim for exercise. I’m no longer felled by bronchitis, and rarely get sick.

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The Importance of Vision Screening

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esearch has found a connection between vision and Alzheimer’s disease. In a study of elderly people over the age of 71, all of whom had normal cognitive functioning at the beginning of the study, those who had undiagnosed or untreated vision problems showed a 9.5-fold increase in the risk of developing Alzheimer’s disease.

Unfortunately, Medicare Parts A and B do not cover routine vision screenings, only a yearly exam for those at high risk for glaucoma. In France, a dementia task force recommends that vision screening be included in all evaluations to prevent Alzheimer’s.

Sleep Apnea and Dementia

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’m also getting treatment for sleep apnea, which I never knew I had. One day a few months ago, I was doing a relaxation meditation lying down, near the edge of sleep, and I felt the tissues of my throat close up and my breathing cut off. For several years, I’ve been exhausted all day despite nine or ten hours of sleep, but if it weren’t for my meditation practice I might never have discovered the sleep apnea. My husband is such a sound sleeper he never noticed if I snored a lot, or if I stopped breathing and startled awake. My only symptoms, aside from extreme fatigue, were frequent headaches first thing in the morning.