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Alzheimer's Research Making Leaps and Bounds

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But, like Thies, she's optimistic. "The way research is going, I think we'll have a much better handle on Alzheimer's disease long before 2050," Morrison-Bogorad tells WebMD.

Thies tells WebMD the missing pieces of the jigsaw puzzle are falling into place on a daily basis. "... But there's still some holes in there about what the initial [problem is] ... that starts the disease," and, he says, we still don't understand the genetics of it.

Morrison-Bogorad says Alzheimer's disease is believed to be spurred by a complex mixture of things that could contribute to the risk of getting the disease -- such as age, genetics, head injuries, high levels of cholesterol in the blood, or heart disease. "It's random luck of the draw," she says.

It's probable that both an environmental and a genetic set of factors determine whether a person gets the disease because two different types of brain abnormalities are characteristics of Alzheimer's. Researchers are unsure if the disease causes these abnormalities, or if the abnormalities cause the disease.

There are two medications in trials now that try to reduce one of these abnormalities -- the plaque build-up in the brain of a protein called beta amyloid.

One drug inhibits an enzyme that's a key step in the formation of beta amyloid. "It's like a cholesterol-lowering" drug, according to Thies. "The other trial is the vaccine trial, where a purified beta-amyloid is given, and its been shown in animals ... that you can decrease the amyloid burden on the brain by giving this vaccination," says Thies.

There is also a lot of work underway on the genetic front. For example, it's known that people who carry a gene that expresses a specific protein called "ApoE4" have a higher likelihood of developing the disease -- but researchers are still unsure why most people who get Alzheimer's disease haven't inherited the gene.

Some scientists are taking their research down to the molecular level, and looking at the cellular abnormalities that could lead to the disease. Researchers at the University of Virginia suggest that abnormal mitochondrial genes -- which are responsible for cells' converting food into usable energy -- may increase the damage caused by naturally occurring elements in the body called oxygen-free radicals. These free radicals, in turn, start a process that ends up creating beta amyloid plaque build-up in the brain.

The importance of this kind of research is that it opens up new avenues for possibly stopping the development of Alzheimer's. "Time will tell," says Morrison-Bogorad.

Another drug being tested, memantine, comes at Alzheimer's disease from a different angle, according to Thies. Memantine is currently used in some parts of the world to treat Parkinson's disease and dementia in the elderly, among other conditions. The drug inhibits the destruction of nerve cells. Results from a trial using this drug on Alzheimer's patients will also be presented at the upcoming World Alzheimer's Congress.

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