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Alzheimer's disease is a progressive brain disorder that destroys the brain's capacity for memory formation and other cognitive function. The most common cause of dementia worldwide, Alzheimer's affects 4.5-5 million adults in the US , and this number is expected to grow to 13 million Americans by the year 2050 if no therapies are discovered. Symptoms of Alzheimer's begin with mild memory problems and end with severe brain damage, debilitating the affected patient. The cause of Alzheimer's disease is currently unknown, however there are changes in the brain that are always associated with the disease. One important change is the formation of plaques (protein deposits) in the brain. These plaques are made up of a protein normally found in the brain called beta ( β ) amyloid. In an Alzheimer's patient, β amyloid accumulates in large amounts forming the plaques. By the time β amyloid plaques form, the patient is usually in the more advanced stages of the disease and very difficult to treat. Interestingly, it is unknown if the plaques cause the symptoms of Alzheimer's disease or if they are only a byproduct of the real culprit. Currently there is no cure for Alzheimer's disease and all treatments used only treat the memory symptoms, not the disease itself. The following study gives some evidence that the accumulation of β amyloid may cause the beginning memory symptoms found in Alzheimer's disease.

Using a strain of mice that is very prone to developing Alzheimer's disease due to the over-expression of genes involved in Alzheimer's, researchers at UCI set out to determine the early processes that may trigger the formation of β amyloid plaques found in the later stages of Alzheimer's. The ability of the mice to learn and remember the correct path through a maze was tested as they aged and researchers found that by 6 months of age, the mice had problems in both short term (figuring out a new maze) and long-term (remembering a maze from day to day) memory. To determine when the memory difficulties began and the state of their brains at the onset of memory loss, the researchers tested the mice in mazes and subsequently examined their brains at various time points. At two months of age, the mice show no memory symptoms and their brains were normal. At four months of age, the mice began to show problems only with their long-term memory. Interestingly, researchers did not see the formation of β amyloid plaques in the brains of these four-month-old mice, however they did find an increase in the protein β amyloid. The researchers in this study then injected antibodies specific for β amyloid into the brain the 4-month-old mice to clear the β amyloid buildup and saw the memory problems disappear. When treatment was withdrawn and β amyloid was allowed to again accumulate, the same memory problems again became apparent. Although this treatment is not currently approved for use in humans, targeting β amyloid appears to be a promising way to treat or postpone this debilitating disease. If β amyloid buildup can be cleared or prevented, this study suggests that symptoms and progression of Alzheimer's disease can be halted.

Other great related material:

http://www.sciencedaily.com/releases/2005/03/050309130709.htm

http://www.alz.org/