To begin Alzheimer’s care, it’s important to form an understanding of the disease. Alzheimer’s disease is the most common form of dementia in the United States. We define dementia as the development of memory and thinking problems, progressive in nature, in an otherwise previously healthy adult. There are many reasons to develop dementia; the most likely is Alzheimer’s disease, but there are other important ones including dementia with Lewy bodies, Parkinson’s disease, multiple strokes, and a variety of other far less common conditions such as brain tumor, infections, normal pressure hydrocephalus, subdural hematomas, etc.
In Alzheimer’s disease we now recognize that the condition begins many years, probably 15-20 years, before it is clinically evident. For this reason, we have changed how we view it so that it is considered present as soon as we can identify any evidence of it in brain studies. Previously, we did not talk about Alzheimer’s disease until there was evident dementia and significant clinical disabilities for the patient. That would have been analogous to thinking that heart disease begins only with a heart attack, rather than the 15, 20, or 30 years during which heart atherosclerosis or deposits of cholesterol and similar substances begin to clog the arteries of the heart and lead to a heart attack. For many years, cardiologists have worked very hard at decreasing the risk for patients with established coronary artery disease, so they do not have a heart attack. In neurology, we are now taking a similar approach trying to identify as early as possible those who are at risk of developing dementia from Alzheimer’s disease or other causes. We are also working at preventing, modulating, or diminishing their risk of expressing the condition. Indeed, it is in this preclinical phase of Alzheimer’s disease when patients are “normal” that we can hopefully make the biggest impact in their long-term outcomes.
We have known for many years that the abnormal deposition of the protein called amyloid is a significant part of the problem in Alzheimer’s disease. Beyond that, other important abnormalities have been found in tau protein in cell-to-cell communications (dendrites), all of which point to a slowly evolving destruction of critical nerve cells in the brain. In our research department, we provide cutting edge treatments that are aimed at decreasing the amyloid burden in brain and allowing the remainder of healthy nerve cells to function to their best capacity. We are also looking at ways of stabilizing the destruction of nerve cells that seems to be tied to the tau protein abnormalities found in many conditions including Alzheimer’s. Regardless of how we get there, it is the lack of connectivity between one brain cell and another that is the final common pathway for loss of memory and loss of function. For that reason, anything we can do to improve brain connectivity to maximize the ability of one nerve cell to talk to another will be beneficial.
We remain committed to scientific, clinically-sound, and patient-oriented care, which is based on the latest neurological and behavioral science.
Michael M. Tuchman, M.D., FAAN