Shedding Light on the Gathering Darkness of Alzheimer's Disease

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Shedding Light on the Gathering Darkness of Alzheimer

The greatest threat to the health and happiness of Baby Boomers in their senior years is Alzheimer’s disease. This ailment causes healthy brain tissue to degenerate, leading to a steady decline in the patient’s ability to learn, remember, reason, and communicate.

While about 5 million Americans now suffer from Alzheimer’s disease, health care experts predict that this number will grow to 8 million by 2030 (when the youngest members of the Baby Boom generation will be 66), and reach 12 million by 2050. Worldwide, nearly 27 million people now have Alzheimer’s, and that number is expected to rise to 100 million by 2050. Without a cure, the Accelerate Cure & Treatments Alzheimer’s Disease Coalition estimates that the Medicare cost to treat U.S. patients will reach $160 billion a year as soon as 2010.1

Currently, there is no cure for the disease, but researchers are working on promising new treatments. Scientists used to think that insoluble plaques of beta-amyloid protein caused the damage to brain cells that led to memory loss. Now, new research suggests that earlier, more soluble forms of beta-amyloid may cause the problem.

Amyloid precursor protein, or APP, is a large protein that is thought to be important to the health of neurons. APP is embedded in the neuronal membrane, residing partly inside and partly outside the cell. At some point, APP is cut into several fragments by three enzymes: alpha-secretase, beta-secretase, and gamma-secretase. In a major breakthrough, scientists recently discovered that, depending on which enzyme does the cutting and where it happens, APP processing can go in two different directions, with dramatically different results.2

In one, considered the usual pathway, alpha-secretase cuts the APP molecule.

This happens within the portion that has the potential to become beta-amyloid. Cutting at this site results in the release into the space outside the neuron of a fragment called sAPPa. This fragment may have beneficial properties, such as promoting neuronal growth and survival. The remaining APP fragment,

still tethered in the neuron’s membrane, is then sliced by gamma-secretase at the end of the beta-amyloid sequence. The smaller of the resulting fragments also is released, while the larger fragment remains within the neuron and is believed to enter the nucleus. No beta-amyloid is produced in this pathway.

However in the second pathway, beta-secretase cuts the APP molecule at one end of the portion that has the potential to become beta-amyloid, releasing a fragment called sAPPa...

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