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2000 Monthly News
November

Elder Services Promotes Lillpopp, Adds Two New Staff
Elder Services awards $35,000 in federal funds for elder support services
New information on Alzheimer’s disease. By Jay Ellis, D.O., F.A.A.N.
Promotion of Nancy McCarthy to Residential Service Coordinator

Medicare to increase payments to nursing homes
Candidate views on Medicare

New information on Alzheimer’s disease. By Jay Ellis, D.O., F.A.A.N.

In the year 2000, there have been several significant advances in the field of Alzheimer’s disease. Last year we discussed the significance of the terms "forgetfullness," "mild cognitive impairment" and "dementia." There has been a great increase in the amount of interest in the category of patients with "mild cognitive impairment," i.e., people who have enough memory loss that they and their loved ones notice a change, but nit so much that it impairs the person’s ability to function in their environment.

Around the world there has been a great emphasis on identification of these individuals to determine whether the progression to Alzheimer’s disease can be interrupted. At a recent Masters Class on Alzheimer’s disease I attended in Cambridge, England, two hours were spent on review of the natural history and the treatment data. Seven studies have been showing a rate of progression to Alzheimer’s between 8 and 15%. Furthermore, biopsies done for various reasons have shown the presence of Alzheimer’s changes in many senior citizens who have not sought medical attention for their memory. It is quite clear that as we age many of us will have the pathpology of Alzheimer’s disease, that is, senile plaques and neurofibrillary tangles. Thus, we need a way to better identify these people clinically and then to intervene. Unfortunately, better clinical identification depends on community response. Intervention studies are being done. We are completing a study of an anti-inflammatory agent and are hoping that the results of this study will be positive. The results of a study performed elsewhere utilizing Celebrex were negative. Out trial should be completed within the next year and a half. In the meantime, we will be initiating another trial utilizing a medicine called galantamine beginning in the winter of 2001. This medication is near market approval for people who already have Alzheimer’s dosease. It appears to have limited side effects and does have effcacy for Alzheimer’s. Agan, we are hoping to find some way to prevent Alzheimer’s in people who are clearly at risk. There is also a European study of a medicine called memantine, which has been approved for use in Germany, but has not yet received approval in the United States.

Another great area of advance has come through the Human Genome Project. We now know that individuals with the early onset of a familial autosomal dominant form of Alzheimer’s have a defect in genes 1, 14 and 21, which cause breakages of amyloid amino acid chains. Amyloid, a chenical protein that circulates in everyone’s blood stream, is associated with the senile plaques od Alzheimer’s disease. We don’t yet know whether the amyloid deposits in dead nerve cells is an end product or causes the nerve cells to die. We do know that amyloid deposits when it is disrupted between certain amino acid sequences. The enzymes causing this cleavage were discovered in 1999 and some pharmaceutical companies already have discovered compounds, which could disrupt that enzyme reaction. Studies in this area possibly will become available in 2001.

In addition, the exciting information about a vaccine against amyloid formation became available early this year. This vaccine offers promise against the formation of amyloid in the brain and the clearing of amyloid already deposited. Work in mice has shown thathtis can be accomplished. Unfortunately, we have no clear idea what effect that would have on the functioning of humans and other organs in the body. Also, since we don’t know whether the amyloid is the cause or the end product of nerve cell death, eliminating the amyloid might not make the person’s cognitive function better. If the nerve cells are already dead, then they are not going to come back because of the removal of amyloid. Trials of the vaccine are slated for the year 2001. The ability to tie together the information frm the genetic studies with the information from the amyloid chemistry studies represents a significant and major step forward. We are still at a loss to use information from the chromosome 19 data, which shows that individuals with certain apolipopretein episilon 4 patterns are more at risk to develop Alzheimer’s than are other individuals. Once we have a way to identify individuals at high risk for Alzheimer’s earlier, then we may be able to utilize that information. Obviously, we need a medication that can interrupt the process before it has already begun.

As to actual treatment for Alzheimer’s patients, the year has seen the approval by the FDA of a new agent called rivastigmine (Exelon) for treatment of patients with mild to moderate Alzheimer’s disease. We were involved in two studies of this agent since 1997. Studies have showed that Exelon improved the activities of daily living, the behavior, and the cognitive status of Alzheimer’s patients. In fact, data now exists showing improvement lasting for as long as two years with slowing of the progression of the decline in Alzheimer’s disease patients. Also, the medication appeared to work for people with more severe disease, as well as for people with only mild disease. This medication appears to be safe with its side effects being nausea, vomiting, diarrhea, occasional weight loss, muscle cramps and occasional headache or abdominal pains. None of the side effects were severe or long lasting with any frequency.

Jay M. Ellis, DO, is a neurologist in Berkshire County. He has created a neuroscience research program and Alzheimer’s support services for evaluation, research and treatment of Alzheimer’s patients. For more information, call 413-400-7128 and he will be glad to discuss your questions.