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Alzheimer's Research for a Cure, Treatment, and Prevention

Alzheimer's Research for a Cure, Treatment, and Prevention

Research into the cause, treatment, and prevention of Alzheimer's disease is progressing at a rapid pace. The Alzheimer's Association is the world leader in Alzheimer research and support. Through the combined efforts of the Association, the scientific community, our federal government, and the pharmaceutical industry, we are gaining significant ground in our longstanding battle to defeat this leading form of dementia. The Alzheimer's Association funding of research now totals more than $165 million since the mid-1980s, making us the largest private, nonprofit funder of research in the world.
The pace of discovery is rapidly accelerating; 95 percent of what we know about Alzheimer's has been discovered in the last 15 years. We now know it is possible to maintain brain health and reduce the risk of dementia by managing lifestyle risk factors: keeping mentally active, staying physically active, staying socially engaged, and following a heart-healthy diet high in antioxidants. Many clinical trials are under way to test drugs with the potential to treat or prevent Alzheimer's. Thousands of top scientists and clinicians around the world are actively engaged in Alzheimer research. Federally funded Alzheimer's Disease Centers provide a nationwide infrastructure to translate research advances into improved care and diagnosis for Alzheimer's.
The National Institute on Aging (NIA) is conducting a wide-ranging genetics study to understand the roles of genes in late-onset Alzheimer's; three genes already have been identified as causing rare, inherited forms of the disease. The NIA's new five-year, $60-million Alzheimer's Disease Neuro-imaging Initiative aims to develop better ways to identify those at high risk for Alzheimer's, track disease progression, and monitor response to treatment.
Alzheimer Research Theories: The theory with the largest following remains the "amyloid hypothesis," which assigns a central role to abnormal processing of amyloid precursor protein (APP), a protein found widely throughout the body, but whose normal function remains unknown. This abnormal processing yields a fragment called beta-amyloid (A), which aggregates by stages into the amyloid plaques that are one hallmark of Alzheimer pathology. Proponents of the amyloid hypothesis see production and aggregation of beta-amyloid as the key event in nerve cell disruption and destruction. Scientists are investigating a number of therapeutic approaches targeting beta-amyloid.
Another active area of research dealing with stroke, spinal cord injury, and other nerve-damaging conditions is nerve growth factors to discover what role nerve damaging conditions play in Alzheimer's disease. Scientists are testing drugs that stimulate production of nerve growth factors, which are proteins that regulate nerve cell maturation, survival, and repair.
The second most prominent Alzheimer theory assigns a causative role to tau, a protein that normally helps organize and stabilize a cell's internal "skeleton." In Alzheimer's, tau deforms and loses its ability to support the cell, eventually creating neurofibrillary tangles--the second hallmark of Alzheimer's pathology (the other hallmark is beta-amyloid plaques).
The focus on inflammation is another area under study. Studies have revealed that individuals taking anti-inflammatory drugs to treat such conditions as arthritis appear to have a lower-than-expected occurrence of Alzheimer's. Scientists have launched several clinical trials to investigate specifically whether use of anti-inflammatory drugs may reduce Alzheimer risk.
Another area of research focuses on the relationship between vascular factors and Alzheimer's. Researchers have long observed that individuals with known cardiovascular risk factors appear to have an increased risk of developing Alzheimer's. Studies suggest that people taking statins, a class of drugs prescribed to lower blood cholesterol levels, may have a lower-than-usual risk of Alzheimer's. Other studies hint that elevated blood levels of the protein building block homocysteine--known to be a risk factor for heart disease--may also increase Alzheimer risk. Further, one form of the gene that codes the cholesterol-carrying protein apolipoprotein E (ApoE), called APOE-e4, is a known risk factor for late-onset Alzheimer's. These lines of evidence all support a link between cardiovascular risk factors and Alzheimer's.
Additional information about current drug trials and opportunities to participate in local research trails may be found on the Alzheimer's Association, Greater Maryland Chapter's website:
The Alzheimer's Association local office is located at 5 Public Square, Suite 307. Office hours are Monday-Friday from 9 a.m. to 5 p.m. The phone number is 301.797.4892. All office staff are trained to assist visitors and callers with issues dealing with Alzheimer's disease. From how to get a diagnosis to dealing with end of life issues, the staff of the Alzheimer's Association can provide assistance.

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