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Columbia Researchers Identify Possible New Culprit in Alzheimer’s Disease Plaque Formation

  [ 49 votes ]   [ Discuss This Article ] • March 10, 2003

A new study from Columbia University College of Physicians and Surgeons (P&S) and Stanford University suggests that the malfunctioning of brain cells called astrocytes may be behind the accumulation of amyloid protein in the brains of patients with Alzheimer’s disease.

Alzheimer’s disease, most researchers believe, is caused when small peptides called beta-amyloid accumulate in the brain. Everyone makes these peptides at all times during their life, but in people with Alzheimer’s, either too much is made or too little is degraded or both. The resulting excess of peptides aggregate together in plaques. Beta-amyloid plaques then lead to death of neurons and dementia.

Researchers have known that microglia cells in the brain, which surround the plaques, can ingest and destroy the plaque’s proteins in cell culture, so they’ve been trying to stimulate the cells to do so in the body. But the role of other cells that surround the plaques, the astrocytes, hasn’t been clear. The new findings show that normal astrocytes can also degrade plaque proteins, suggesting that treatments to boost astrocyte activity in Alzheimer’s disease may be beneficial.

The study is published in the advanced online edition of Nature Medicine and will be featured in the April issue of the publication.

“This is the first study to show that astrocytes can remove beta-amyloid deposits from brain tissue,” says the study’s senior author, Dr. Jens Husemann, associate research scientist in the Department of Physiology and Cellular Biophysics at P&S. “In addition, astrocytes outnumber microglia in the brain, so they may be very important. Now researchers will explore ways to activate astrocytes to increase beta-amyloid removal.”

“This study contributes to our knowledge of the function of these immune processes, information that may provide opportunities to develop better treatments,” says Dr. Bill Thies, vice president of medical and scientific affairs at the Alzheimer's Association, one of the sponsors of this research. (The work was also supported by the Alzheimer's Disease Research Center at Columbia University and the National Institute on Aging.)

The researchers also speculate that Alzheimer’s disease may result from problems with the astrocytes. It is still unknown why beta-amyloid accumulates in people with the late-onset form of the disease, but one possibility is that the astrocytes fail to degrade the proteins. Dr. Husemann and his colleagues are now looking at astrocytes from the brains of Alzheimer’s patients and mice with a similar disease to see if the cells are still capable of destroying beta-amyloid.

In the Nature Medicine study, the researchers found that astrocytes ingest beta-amyloid when they placed cultured adult mouse astrocytes onto brain tissue taken from Alzheimer’s model mice. The cells reduced the amount of beta amyloid in the brain tissue by 40 percent during the 24-hour experiment.

To see if the astrocytes also degraded the protein, they kept track of the protein in astrocytes cultured in broth. At the beginning of the incubation, all protein was in the broth. In the next 24 hours, the researchers saw that all of the protein moved into the cells, and then disappeared completely, indicating the cells had degraded the beta amyloid and not exported it.

Though the researchers suggest that improving astrocyte’s ability to degrade beta-amyloid may be therapeutic, they also caution that other astrocyte functions may contribute to the disease. “Some people think that if the cells don’t migrate to plaques, the astrocytes may not release inflammatory molecules that damage the surrounding brain tissue,” Dr. Husemann says. “It will be a delicate balancing act to stimulate plaque removal while keeping inflammation down at the same time.”

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