Featured Research

from universities, journals, and other organizations

Columbia University Researchers Identify Possible New Culprit In Alzheimer's Disease Plaque Formation

Date:
March 12, 2003
Source:
Columbia University College Of Physicians And Surgeons
Summary:
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.

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 vivo. 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 research group, including Dr. Samuel Silverstein, John C. Dalton Professor of Physiology & Cellular Biophysics at P&S, Dr. John Loike, research scientist in the Department of Physiology & Cellular Biophysics at P&S, and Dr. Tony Wyss-Coray, assistant professor of neurology at Stanford University, also speculates 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."


Story Source:

The above story is based on materials provided by Columbia University College Of Physicians And Surgeons. Note: Materials may be edited for content and length.


Cite This Page:

Columbia University College Of Physicians And Surgeons. "Columbia University Researchers Identify Possible New Culprit In Alzheimer's Disease Plaque Formation." ScienceDaily. ScienceDaily, 12 March 2003. <www.sciencedaily.com/releases/2003/03/030312072322.htm>.
Columbia University College Of Physicians And Surgeons. (2003, March 12). Columbia University Researchers Identify Possible New Culprit In Alzheimer's Disease Plaque Formation. ScienceDaily. Retrieved July 24, 2014 from www.sciencedaily.com/releases/2003/03/030312072322.htm
Columbia University College Of Physicians And Surgeons. "Columbia University Researchers Identify Possible New Culprit In Alzheimer's Disease Plaque Formation." ScienceDaily. www.sciencedaily.com/releases/2003/03/030312072322.htm (accessed July 24, 2014).

Share This




More Mind & Brain News

Thursday, July 24, 2014

Featured Research

from universities, journals, and other organizations


Featured Videos

from AP, Reuters, AFP, and other news services

New Painkiller Designed To Discourage Abuse: Will It Work?

New Painkiller Designed To Discourage Abuse: Will It Work?

Newsy (July 24, 2014) The FDA approved Targiniq ER on Wednesday, a painkiller designed to keep users from abusing it. Like any new medication, however, it has doubters. Video provided by Newsy
Powered by NewsLook.com
China's Ageing Millions Look Forward to Bleak Future

China's Ageing Millions Look Forward to Bleak Future

AFP (July 24, 2014) China's elderly population is expanding so quickly that children struggle to look after them, pushing them to do something unexpected in Chinese society- move their parents into a nursing home. Duration: 02:07 Video provided by AFP
Powered by NewsLook.com
Idaho Boy Helps Brother With Disabilities Complete Triathlon

Idaho Boy Helps Brother With Disabilities Complete Triathlon

Newsy (July 23, 2014) An 8-year-old boy helped his younger brother, who has a rare genetic condition that's confined him to a wheelchair, finish a triathlon. Video provided by Newsy
Powered by NewsLook.com
Huge Schizophrenia Study Finds Dozens Of New Genetic Causes

Huge Schizophrenia Study Finds Dozens Of New Genetic Causes

Newsy (July 22, 2014) The 83 new genetic markers could open dozens of new avenues for schizophrenia treatment research. Video provided by Newsy
Powered by NewsLook.com

Search ScienceDaily

Number of stories in archives: 140,361

Find with keyword(s):
Enter a keyword or phrase to search ScienceDaily for related topics and research stories.

Save/Print:
Share:

Breaking News:
from the past week

In Other News

... from NewsDaily.com

Science News

    Health News

      Environment News

        Technology News



          Save/Print:
          Share:

          Free Subscriptions


          Get the latest science news with ScienceDaily's free email newsletters, updated daily and weekly. Or view hourly updated newsfeeds in your RSS reader:

          Get Social & Mobile


          Keep up to date with the latest news from ScienceDaily via social networks and mobile apps:

          Have Feedback?


          Tell us what you think of ScienceDaily -- we welcome both positive and negative comments. Have any problems using the site? Questions?
          Mobile: iPhone Android Web
          Follow: Facebook Twitter Google+
          Subscribe: RSS Feeds Email Newsletters
          Latest Headlines Health & Medicine Mind & Brain Space & Time Matter & Energy Computers & Math Plants & Animals Earth & Climate Fossils & Ruins