Post by charlie0 on Jan 21, 2005 7:38:34 GMT -5
This article appeared in the St. Louis Post-Dispatch.
Researchers work to reverse Alzheimer's
By Tina Hesman
Of the Post-Dispatch
01/20/2005
Some symptoms of Alzheimer's disease may be reversible, suggests new research from Washington University.
In experiments with mice, a team of researchers led by Robert P. Brendza and Dr. David Holtzman found that removing some of the brain-damaging plaques associated with the disease reduced swelling in nerve fibers. The discovery is the first evidence that some types of nerve damage caused by the disease can be undone, researchers say.
The result is probably good news for Alzheimer's disease patients and their families. It may mean that new drugs and therapies to halt or reduce buildup of plaques could improve some disease symptoms.
About 4.5 million people in the United States have the debilitating memory-robbing disease, and the number is expected to grow as the population ages.
The results of the study will appear in the Journal of Clinical Investigation on Feb. 5.
Neuroscientists have long thought that nerve damage, such as that caused by Alzheimer's and other diseases, was permanent, said Samuel Gandy, director of the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia.
"It was an assumption based on no good data, frankly," Gandy said.
The Washington University researchers wanted to see if removing toxic proteins from the brains of mice with an Alzheimer's-like disease could stop further damage, Brendza said.
"We didn't know it would even do that," he said.
He injected antibodies into the brains of mice with the disease. The antibodies attacked and removed about half the amount of a protein called beta-amyloid or A-beta from the mice's brains. That protein sticks together, forming fibers and plaques that damage the brains of people and animals with Alzheimer's disease.
Long fibers, called axons and dendrites, extend from the main parts of brain cells and form connections, called synapses, that allow neurons to communicate. When A-beta plaques form around the neurons, axons and dendrites get irritated and damaged. The damage is visible in the form of swollen bulbs, Brendza said.
Brendza thought that using the antibodies to clear away A-beta could stop more bumps from forming on the nerves. But within three days of injecting the antibodies, the number of swollen areas went down and some of the remaining bulbs deflated. In other words, the nerves got better.
Over the course of a week about 25 percent of the swellings went away or shrank in volume, Holtzman said.
"I didn't think it was going to be a reversible change," he said.
The recovery was not complete, but some additional improvement might happen over time, said John Hardy, chief of the Laboratory of Neurogenetics at the National Institutes of Health's National Institute on Aging.
"I think it's an important observation that the disease is at least partially reversible," Hardy said.
No one knows whether antibody therapy could help people with Alzheimer's disease. Clinical trials of antibodies against beta-amyloid were halted when some people developed serious side effects. But scientists are now testing a variety of drugs aimed at stopping plaque formation or breaking them up, Gandy said.
"This validates all the other anti-amyloid approaches that are going on right now," he said.
Researchers work to reverse Alzheimer's
By Tina Hesman
Of the Post-Dispatch
01/20/2005
Some symptoms of Alzheimer's disease may be reversible, suggests new research from Washington University.
In experiments with mice, a team of researchers led by Robert P. Brendza and Dr. David Holtzman found that removing some of the brain-damaging plaques associated with the disease reduced swelling in nerve fibers. The discovery is the first evidence that some types of nerve damage caused by the disease can be undone, researchers say.
The result is probably good news for Alzheimer's disease patients and their families. It may mean that new drugs and therapies to halt or reduce buildup of plaques could improve some disease symptoms.
About 4.5 million people in the United States have the debilitating memory-robbing disease, and the number is expected to grow as the population ages.
The results of the study will appear in the Journal of Clinical Investigation on Feb. 5.
Neuroscientists have long thought that nerve damage, such as that caused by Alzheimer's and other diseases, was permanent, said Samuel Gandy, director of the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia.
"It was an assumption based on no good data, frankly," Gandy said.
The Washington University researchers wanted to see if removing toxic proteins from the brains of mice with an Alzheimer's-like disease could stop further damage, Brendza said.
"We didn't know it would even do that," he said.
He injected antibodies into the brains of mice with the disease. The antibodies attacked and removed about half the amount of a protein called beta-amyloid or A-beta from the mice's brains. That protein sticks together, forming fibers and plaques that damage the brains of people and animals with Alzheimer's disease.
Long fibers, called axons and dendrites, extend from the main parts of brain cells and form connections, called synapses, that allow neurons to communicate. When A-beta plaques form around the neurons, axons and dendrites get irritated and damaged. The damage is visible in the form of swollen bulbs, Brendza said.
Brendza thought that using the antibodies to clear away A-beta could stop more bumps from forming on the nerves. But within three days of injecting the antibodies, the number of swollen areas went down and some of the remaining bulbs deflated. In other words, the nerves got better.
Over the course of a week about 25 percent of the swellings went away or shrank in volume, Holtzman said.
"I didn't think it was going to be a reversible change," he said.
The recovery was not complete, but some additional improvement might happen over time, said John Hardy, chief of the Laboratory of Neurogenetics at the National Institutes of Health's National Institute on Aging.
"I think it's an important observation that the disease is at least partially reversible," Hardy said.
No one knows whether antibody therapy could help people with Alzheimer's disease. Clinical trials of antibodies against beta-amyloid were halted when some people developed serious side effects. But scientists are now testing a variety of drugs aimed at stopping plaque formation or breaking them up, Gandy said.
"This validates all the other anti-amyloid approaches that are going on right now," he said.