Cognitive Disorders in Later Life

An Interview with Steven T. DeKosky, M.D.

Portrait of Dr. DeKosky
© Tom Cogill

Steven T. DeKosky, M.D., principal investigator and lead author of the Ginkgo Evaluation of Memory study, is vice president and dean of the University of Virginia School of Medicine. He was formerly professor and chairman of the department of neurology and director of the Alzheimer's Disease Research Center at the University of Pittsburgh. Dr. DeKosky's research has progressively focused on the science and clinical care of Alzheimer's disease. Among his other commitments, he has served as a board member for the Alzheimer's Association USA and Alzheimer's Disease International.

Why do some older Americans turn to CAM to try to prevent or treat cognitive issues? How do you advise your patients in this situation?

Older individuals notice the normal age-related changes in memory and cognitive function. This can serve as a stimulus to try things that may be helpful in preserving their thinking function, including many preparations that may have a biological rationale [i.e., a theory as to how it may work], such as anti-inflammatory or antioxidant activity. We know that there is mild inflammation and oxidative stress in the brain (and other parts of the body) associated with normal aging.

In general, if a CAM medication that a patient wishes to try is not harmful and is not expensive to the point of causing family hardship, I will work to incorporate its use along with FDA-approved medications, as will many physicians. The major problems are if side effects emerge or if it interacts, or could interact, with a prescription medicine. Thus, it is very important for patients to tell their doctors about all medications—both over-the-counter and prescription—that they are taking.

I also tell patients that it is helpful if there is a biological rationale for a CAM treatment, but it does not prove the treatment works. If there are clinical trials evaluating the treatment, I urge the patient and family to participate, both for the careful evaluation and follow-up that is provided and to help science to determine whether or not the treatment truly is effective.

You have also researched depression in later life. Is this a common problem, and can it be connected to cognitive disorders?

Depression is quite common in late life. It is quite capable of causing both loss of interest in everyday activities and impairment of memory, thinking functions, and speed of cognitive processing. It should always be a consideration in the differential diagnosis of cognitive impairment in late life. The literature is still unsettled as to whether having depression is a risk factor for Alzheimer's disease or whether some of the early brain changes in Alzheimer's cause depression. In either case, looking for depression and treating it aggressively is extremely important.

There are other disorders as well that interact with Alzheimer's and other cognitive losses in late life; perhaps the most frequent is cerebrovascular disease. Vascular disease and large and small strokes can in themselves cause vascular dementia. Also, it appears that the presence of Alzheimer's pathology and cerebrovascular disease interact. Many experts think that clinical dementia symptoms emerge sooner if you have both diseases present.

"Depression is quite common in late life… [it] should always be a consideration in the differential diagnosis of cognitive impairment."
—Dr. DeKosky

As an expert in Alzheimer's disease, what do you think are some promising and/or exciting directions in that field?

The initial medications developed for Alzheimer's emerged because we understood some of the losses of specific neurotransmitters, the chemicals that allow nerve cells to communicate with each other. Boosting or enhancing neurotransmission was intended to give some short-term symptomatic improvement. That strategy worked, but was not directed at trying to slow progression of the disease.

Over the last decade, research has increasingly shown us the fundamental mechanisms that appear to result in loss of brain cells and their connections and to affect and alter proteins. An immense amount of research is being directed toward trying to stop the changes in specific proteins and actually modify the course of the disease process. Several of these new medications are in clinical trials now. Recent, spectacular improvements in neuroimaging will not only improve our diagnostic capability but will allow us to measure brain structure or function over time to see whether the brain is shrinking less and its function is maintained. This will make our trials much more efficient and hopefully shorter, and put less stress on our patients.

When medications have been shown to help people who have symptomatic Alzheimer's disease, they will likely go into trials in older people who are cognitively normal or have only very mild cognitive impairment, to see if they can prevent symptoms from ever emerging or delay them for so long that they never become a factor in someone's normal lifespan. That is our ultimate goal.

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