Keystone Symposia gives an update on Alzheimer’s disease
A couple of months ago, Keystone Symposia hosted a community forum on Alzheimer’s disease at Colorado Mountain College in Breckenridge. The speakers were all leading research scientists drawn from the Keystone Symposia conference “Alzheimer’s Disease — From Fundamental Insights to Light at the End of the Translational Tunnel” held at the Keystone Conference Center. I was struck in several ways by the event. First, it was very well attended; far more people turned up than we had anticipated despite the rather lousy weather that night. This attests to the fact that so many people are touched by the disease, either as a sufferer, caregiver or relative. Second, the quality of the audience’s questions was remarkably sophisticated, a fact much appreciated by the speakers. This again attests to the prominence of the disease in our culture. And third, it was unfortunately clear that there is no cure for Alzheimer’s, though considerable progress in understanding the disease is being made. Indeed, the speakers at the forum are some of the leading Alzheimer’s researchers and will be at the forefront in developing future treatments or possibly cures.
Alzheimer’s is an awful disease that can progressively rob patients of their memory and cognitive skills. In the disease’s latter stages, patients lose the ability to perform even simple daily activities and end up requiring full-time care. Of particular concern is the prevalence of the disease, with current estimates of more than 5 million sufferers in the United States alone. It is the nation’s sixth leading cause of death. The causes and underlying mechanisms of Alzheimer’s are not known. Although it is typically diagnosed in people over 65 years of age, researchers do understand that Alzheimer’s is a disease and not part of the normal aging process.
Alzheimer’s behaves in many ways like an infection that progressively spreads from cell to cell in the brain. Diseased areas are characterized by amyloid plaques (insoluble deposits of beta-amyloid protein in between neurons) and neurofibrillary tangles (aggregates of tau protein within neuronal cells) that can be visualized by microscopy in the brains of cadavers. Much attention has focused on the tau protein since scientists believe that the accumulation of an abnormal and non-functional form of tau may cause the death of affected nerve cells. Unfortunately, the mechanism by which abnormal tau is transmitted from cell to cell is not understood, nor is it known whether tau tangles are the cause or consequence of the disease.
Recent studies may be shedding light on this important question and perhaps point to possible future treatments. Researchers have created genetically engineered mice that express the abnormal form of the tau protein in a specific region of the brain. They were then able to show that the damaged tau protein could “infect” surrounding cells and induce tangles within them. This led to the conclusion that damaged tau either moves from one neuron to another, or somehow induces the damage of tau in neighboring cells. In either case, this leads to tau aggregation and subsequent cell death. These new findings advance our understanding of how the disease progresses, but do not address the initial triggers. The findings nevertheless point to treatment possibilities. For example, the Alzheimer’s Society in the U.K. funds research on the capacity of lithium to protect nerve cells by causing tau to accumulate in rounded clumps that are less likely to cause damage to the cell. Other treatments that target tau are showing promise in improving neuron function and cognition in animal models of Alzheimer’s disease.
A major challenge in understanding Alzheimer’s remains the lack of a definitive clinical test; diagnoses instead have to be made through cognitive testing. Currently there is excitement that changes in the retina and lens of the eye that develop in Alzheimer’s patients may provide a “window” into the disease. A simple eye exam might allow physicians to identify patients at the very earliest stages of the disease, though the jury is still out. And the value of a diagnostic tool may be limited to research studies given that there is currently no cure. The same dilemma exists with genetic testing. Individuals who carry the ApoE4 gene have a much higher likelihood of developing Alzheimer’s but worry there is not much they can do with the knowledge.
There is some evidence that simple lifestyle improvements we can all make, such as exercise and diet, might delay the onset and reduce the severity of Alzheimer’s. For now, the awareness that we can all develop this disease but perhaps lessen its blow will be our best defense.
David L. “Woody” Woodland, Ph.D., is the chief scientific officer of Silverthorne-based Keystone Symposia on Molecular and Cellular Biology, a nonprofit dedicated to accelerating life science discovery by convening internationally renowned research conferences in Summit County and worldwide. Woody can be reached at (970) 262-1230 ext. 131 or firstname.lastname@example.org.
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