New Leads In The Fight Against Alzheimer’s Disease
Dementia is a general term to describe the decline in mental activity severe enough to interfere with daily activities. There are several types of dementia, although Alzheimer’s disease is the most common type, accounting for an estimated 60 to 80 percent of cases.
Although some medicines are palliative, none is able to cure the disease. Fortunately now a recent discovery may change the outlook of this disease and eventually to its cure.
It is estimated that 5.4 million Americans are living with Alzheimer’s today, and their care involves approximately 15 million people at an annual cost of 183 million dollars. While deaths by HIV/AIDS, stroke and heart disease have diminished in the last several years, deaths due to Alzheimer’s have steadily increased and now every 69 seconds somebody in the U.S. develops the disease.
When in 1901 Dr. Aloysius “Alois” Alzheimer, a German Psychiatrist and neuropathologist observed some unusual behavioral symptoms on Auguste Deter, a patient at the Frankfurt Asylum, he didn’t realize that later he would give his name to a devastating disease: Alzheimer’s disease. Until he died in 1906, Mrs. Deter would become Dr. Alzheimer’s obsession. He could not forget the bizarre symptoms exhibited by her, such as behavior changes, disorientation, confusion and impaired judgment.
Soon after Mrs. Deter’s death, and with the help of two Italian physicians, Dr. Alzheimer used staining techniques to identify two crucial findings in the brain of people affected by Alzheimer’s: some abnormal clumps of protein fragments called beta-amyloid plaques, and disordered neurofibrillary tangles (twisted fibers composed largely of the protein called tau that build up inside nerve cells) which are two of the main features of the disease.
On November 3 of 1906, in a speech in front of medical colleagues, for the first time he presented together the symptoms and the pathology of the disease. A critical chapter had been opened in the search for its understanding. Regrettably, his contribution to the study of Alzheimer’s disease stopped in December of 1915 when he fell ill on his way to the University of Breslau, Silesia, where he had been professor of psychiatry since 1912.
The high levels of beta-amyloid plaques and neurofibrillary tangles make it hard for the brain cells to communicate with each other. Although both substances are hallmarks of the disease, there is no agreement among scientists if they are a byproduct or if they cause the disease. The cells of the hippocampus, which is the center of learning and memory in the brain, are the first to be damaged, and that is why memory loss is one of the first symptoms of Alzheimer’s.
Fortunately since Alzheimer’s original studies there has been steady progress. A recent finding has considerably raised expectations for a cure. A group of researchers at Case Western Reserve University in Ohio found that a cancer drug they have been testing in mice was able to destroy the plaques found in the brains of people affected with Alzheimer’s. Although many drugs that are successful in mice fail to work when tried on people, this finding is reason for optimism.
Normally in the body, the removal of beta-amyloid is carried out by a substance called apolipoprotein E, or ApoE. However, people have many different versions of this protein, one of which, called ApoE4, is one of the biggest risk factors for developing Alzheimer’s. Using a drug called bexarotene, the scientists were able to reduce the levels of beta-amyloid in mice.
After a single dose, the levels of beta-amyloid in the brain were rapidly lowered within six hours, and a 25% reduction was sustained for 70 hours. In older mice with more established beta-amyloid plaques, after seven days of treatment the number of plaques was reduced to a half. What makes this experiment particularly interesting is that after treatment the mice showed improvements in brain function, nest building, maze performance and remembering electrical shocks.
One of the researchers, however, cautioned that although the study had been particularly rewarding and offered great promise, the drug had been tested in only “three mouse models” which simulate the early stages of the disease but are not Alzheimer’s. For a disease like this, which has caused so much damage and concern over the years, even these preliminary news are already good news.
Dr. Cesar Chelala is an international public health consultant.
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