People with Alzheimer's
Alzheimer's Disease
Alzheimer's Disease is a progressive nervous system disorder that affects approximately half of the elderly population over age 85 and roughly 5.2 million people in the United States. It is the sixth leading cause of death in the United States, and is the most commonly associated with brain disruption in older people. The disease, which usually begins after the age of 65, affects the parts of the brain that control thought, memory, and language. Three percent of men and women ages 65 to 74 have the disease, and nearly half of those age 85 and older may have it. It steals victims’ memories, changes their personalities, and renders them speechless and unable to think coherently. But what make the disease so frightening are not just its symptoms but its prevalence. One in 10 people older than 65 suffers from AD; above 85, by some estimates, the odds rise to almost 50%.
Research done and progress so far
Research suggests as many as half of Alzheimer's sufferers may be in the disease's early stages. Diagnosis can be difficult. There is no single test for dementia. But early detection gives people a chance to plan for their future care while they still have the mental capacity to do so. A handful of experimental drugs are being tested for their potential to slow Alzheimer's by fighting the buildup of its hallmark brain plaque, called amyloid; Perhaps more important is testing the brains of healthy elderly people and those with mild memory problems to determine what changes signal impending Alzheimer's — so-called biomarkers that remain a critical gap in scientific understanding. The search continues for another type of diagnostic: genes that predict someone’s risk of Alzheimer’s. So far, three genes— Presenilin 1 (PS1), Presenilin 2 (PS2), and APP—have been linked to rare, early-onset forms of the disease that usually strike people before they reach age 60; each child of such a patient stands a 50% chance of inheriting the gene and thus succumbing to the disease if he or she lives long enough (7-12). And one version of a fourth gene, ApoE, increases a person’s risk of AD. Research activity on AD has been quite phenomenal. Its rapid progress is demystifying the disease. The past decade’s insights into the genetics and underlying biological processes of the illness have proved to be very beneficial.
Future holds promise
Several different strategies for alleviating or preventing some of the symptoms of AD are being assessed now, and other lines of research are pointing to additional disease-fighting strategies. Research regarding the specific processes involved in the ß-amyloid (Aß) protein and its role in the early phases of Alzheimer's. The secretion of Aß in the beginning stages of AD, appears to be the major cause of plaques (formations or growths) in the brain. Another approach predicts that these proteins, some dissolved in serum and others embedded on the surfaces of circulating red and white blood cells are collectively called "complement".
The primary function of complement is to defend the body against infection. Through the cooperative actions of its component proteins, complement not only recognizes and kills invading microorganisms, it also attracts and directs the action of cells at sites of injury and infection, and augments ("complements") the antibody response to invasion. Hence complement is important in both inflammation and the antibody response of the immune system. Several studies showing that certain types of painkillers—non steroidal anti-inflammatory drugs (NSAIDs), which include aspirin and ibuprofen but not acetaminophen—delay the onset of AD. Other epidemiological studies have uncovered promising hints that estrogen replacement therapy might protect women from Alzheimer’s.
US Alzheimer's death rate per 100,000 by Age.
Other ongoing clinical prevention trials will assess the protective effects, if any, of elements such as vitamin E and ginkgo biloba. Experiments have shown that administration of vitamin E in people with established AD delayed their entry into nursing homes, a major milestone in the progression of the disease. The AD-prevention hypothesis dearest to the hearts of many researchers goes by several different names: the cognitive reserve hypothesis, the cortical reserve hypothesis, and the “use it or lose it” hypothesis. According to the theory, stimulating the brain, say, by regularly reading research or introductory review articles, decreases the risk of developing Alzheimer’s. Some findings suggest that stimulating environments, exercise and diets low in calories might reduce the effects of AD. Drugs are also in development that target specific areas responsible for the degeneration. One promising approach for treating and preventing AD is based upon stimulating the immune system to remove the amyloid from the brain.
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