We can beat Alzheimer’s crushing burdens on families and society—and help may be here soon.

I have devoted my professional life to finding treatments—and, I hope, someday cures—for malignant brain tumors, because I always have thought nothing could be worse than a diagnosis of brain cancer. The brain and its thought- and emotion-processing centers give us our unique personalities and define who we are. Having our sense of self taken away in a life-and-death battle is hard to fathom.

Yet, as cruel as brain cancer is, I have come to believe that Alzheimer’s disease is worse. I know firsthand its devastating effects because it took my mother’s life just before Memorial Day. For the past few years, I could do nothing but watch as this bright, retired school teacher lost the ability to communicate, care for herself, or recognize her family.

With brain tumors, as long as we can keep the cancer in remission, a patient will have a fairly good quality of life until the very end. The worst time usually is a matter of just a few months, so the period of “good” versus that of “not good” is better for cancer than Alzheimer’s patients; they face a long steady decline, usually lasting four to eight years—sometimes as long as two decades.

Watching my mother’s struggle and seeing and feeling the effects on me and our family, I know that we must find answers to the malicious riddles of Alzheimer’s. My passion is fueled by my inability to intervene. It is too late for my mother, but I believe we soon can have therapies in place for my kids’ and grandkids’ generations.

Beyond the personal level, Alzheimer’s disease strains our society and health care system. If we fail to solve this problem—as the population continues to age—Alzheimer’s alone has the potential to bankrupt Medicare. The Alzheimer’s Association says 75% of those afflicted will be admitted to nursing homes by age 80, compared with four percent of the general population. The government, aware of the dire forecasts, is taking action: Health and Human Services Secretary Kathleen Sebelius has announced the creation of a National Alzheimer’s Plan focused on creating treatments and providing help for patients and families. Critical problems exist in our understanding of, and approach to, Alzheimer’s. Addressing them gives us the opportunity to reverse our approaches.

We now diagnose this disease when people develop memory loss when they start forgetting how to get to their friend’s house, where they parked their car or left their keys. However, the disease process begins 10, 15, or 20 years before symptoms start. By the time we see memory loss, patients already have lost 40% to 50% of their brain cells, which, essentially, is at the end stage of the disease.

Our diagnostic tools also are crude, little more than IQ tests to detect problems with memory and comprehension. The way we diagnose the disease inherently is inaccurate, so what we call Alzheimer’s may not always be. It may be vascular dementia from ministrokes that have occurred over time or frontotemporal dementia, which is totally different. Several disorders and disease processes can cause cognitive issues that may look like those associated with Alzheimer’s.

When Dr. Alois Alzheimer in 1906 looked during autopsy procedures at brains of patients who died after suffering a specific type of mental confusion and deterioration, he found unusual clumps and fibers of proteins. These sticky substances—plaques consisting of beta-amyloid protein and neurofibrillary tangles of tau protein—remain the hallmark of Alzheimer’s disease. The proteins do not show up on CT or MRI scans. Although early detection is an area of great research interest, we still have no practical, humane, or accurate way to view these plaques while a patient lives. Just as in 1906, autopsy provides the only definitive diagnosis of Alzheimer’s. To advance our care, we must find a way to make the diagnosis early and accurately.

At Cedars-Sinai Medical Center, we have discovered that beta-amyloid protein plaques occur not only in the brain, but in the retina in the back of the eye. Our research shows they can be seen in the retina even before they begin to accumulate in the brain. With this discovery, we developed a device that enables us to look through the eye—just as an ophthalmologist does to diagnose retinal disease—and see these amyloid plaques. This may give us a quick, inexpensive, and noninvasive way to screen patients for Alzheimer’s disease early in the destructive process. Based on good results in laboratory studies, we are working with major pharmaceutical companies to test this technology in patients. Those who develop drugs are interested in early detection because treatments have a much better chance of success if they can be started earlier rather than later.

A good example of this is the disease process of diabetes. If you have diabetes and it is detected early, steps can be taken to control blood glucose levels, which are likely to prevent progression to kidney failure, vision loss, and other potential effects of long-term high sugar levels. On the other hand, if you go see a physician after having uncontrolled diabetes for 10 or 20 years, and you already have kidney failure, you might be able to gain control of your blood sugar, but you cannot reverse the damage that has been done.

Similarly, we are trying to move the focus of Alzheimer’s disease back to the early stage where intervention can help. I am convinced we can do this in just a few years. While cancer, my lifetime research focus, is hard to treat—we essentially have to remove or kill 100% of cancer cells because, if we leave even one or two percent, they can divide and the cancer can grow back—with Alzheimer’s, the only thing we must do is slow its destruction, a much easier objective.

Keep in mind that damage begins years before Alzheimer’s symptoms start to emerge. Now, imagine a person who begins the harms at 50 and will start to have memory loss at 75. If we can slow that process by half, so that memory loss begins at 100, that practically is a home run. The vast majority of patients with Alzheimer’s would live out their natural lives without suffering the disease’s consequences rather than spending their final four to 20 years in a nursing home unable to recognize family members and loved ones. Before my mother passed, she had no quality of life. When she could express herself, she made it clear that she did not want to go on this way. Although her mind was taken early, her body lived on.

I believe the studies are correct: Alzheimer’s disease taxes caregivers more than patients themselves. It is not surprising that 61% of family caregivers rate the emotional stress as high or very high. One-third report symptoms of depression and statistics also reflect the great stress on family finances and relationships. Trying to deal with my mother’s needs became 100% of my father’s focus, and he—an 88-year-old diabetic—has health issues of his own.

We tried to maintain my parents’ independence, hiring caregivers to be there eight hours a day, then 16. As my mother lost her ability to do her activities of daily living, we needed someone around the clock, which is extremely expensive. When she required more caregivers to bathe her, cook for her, and feed her, we needed to move her to a skilled assisted living facility. My father, who has no mental impairment, had to go with her, living in a place where most of the residents have some type of dementia.

It is all draining and tragic. It is a classic example of the disease’s all-consuming impact on families. The latest data from the Alzheimer’s Association says 65% of caregivers have to take time off work; 20% have to take a leave of absence; 13% dropped to part-time work; and 11% have to give up working entirely. Daughters more often than sons stop working to become primary caregivers, adding another layer of emotional, physical, and financial strain.

The protein deposits that Dr. Alzheimer found more than 100 years ago remain something of a mystery. We know they kill nerve cells in the brain and we think that, by reducing the amount of plaque, we can lessen the effects of the disease. Pharmaceutical companies are focusing their research on developing drugs to prevent this accumulation in the brain.

We also know that Alzheimer’s is a complex disease. It is not just a matter of protein plaques and neurofibrillary tangles. An intense inflammatory cascade takes place. I think the immune system is at the center of the basic mechanisms of the disease and it will play a critical role in the solution.

At present, we are studying three methods of manipulating the immune system and, in pre-clinical models—laboratory and lab rat studies—we see that, if we manipulate the inflammation that is occurring in the brain, we can slow disease progression significantly.

Still, there are things many of us can do now to improve our odds against Alzheimer’s. Going back to the diabetes analogy, insulin can be used to control high blood sugar but, by making certain lifestyle changes, many people can avoid becoming diabetic. We lack a therapy like insulin to treat Alzheimer’s, but we are beginning to understand that risk factors for the disease are very similar to those for diabetes, stroke, and heart disease.

What is good for the heart appears to be good for the brain: reducing fats, simple carbohydrates, sugars, and salt in the diet; increasing intake of fruits and vegetables; eliminating excess body fat; and increasing exercise. Studies suggest that getting regular exercise may be the single most important thing you can do to improve your odds against Alzheimer’s disease.

We may be able to make a dent in the Alzheimer’s statistics—even before the discovery of a magic bullet, and especially if we can identify at-risk patients early—by encouraging the adoption of lifestyle choices that may help defend against the disease.

As a neurosurgeon working every day with patients suffering from brain tumors and other serious disorders, I keenly am aware that life is quite fragile and precious. Confronting a devastating medical issue always puts the relative value of material things into perspective. It gives us a chance to refocus on what life really means. Watching my mother lose her ability to speak, remember, and recognize her loved ones was very, very tough, but it strengthened my resolve to help find a cure for this disease. Now, it is personal.

Keith L Black is chair and professor in the Department of Neurosurgery at Cedars-Sinai Medical Center; Los Angeles, Calif.