Study also notes that related neuronal damage follows soon after
WEDNESDAY, Feb. 6 (HealthDay News) -- An advanced imaging study has captured the fact that amyloid plaques, the harbingers of Alzheimer's disease, can develop in just 24 hours.
"They form more rapidly than expected," said Dr. Bradley Hyman, leader of the group reporting the finding in the Feb. 7 issue of Nature. Once the plaques develop, damage is evident in nearby nerve cells almost immediately, he added.
"The study we've done, using an animal model of Alzheimer's disease, tried to sort out the order in which things occur," said Hyman, director of the Alzheimer's Unit at the Massachusetts General Hospital Institute for Neurodegenerative Disease. "We've had snapshots of individual steps in the past. This microscopic technology gives us the ability to watch the process from beginning to end, to see the variety of things that happen as inflammatory cells get activated."
The microscopic imaging, done first weekly and then daily, found that plaque formation was a relatively rare event. But plaques could be seen in some animals in as little as 24 hours after a plaque-free image was taken.
What happens in the animals, mice bred to develop amyloid plaques, almost certainly happens in the human brain, Hyman said, and the finding could be applied to humans at risk for developing Alzheimer's.
"Knowing that plaque occurs quickly implies that something initiates it," he said. "That is the next question to be answered."
The studies showed that nerve cell changes associated with Alzheimer's disease appear within days. The results confirm suspicions that plaque formation is a primary event in the abnormal cell activity that underlies Alzheimer's disease, Hyman said.
"Watching the pathology unfold in real time dynamically, that is an extremely exciting move forward," said Dr. Sam Gandy, chairman of the Alzheimer's Association medical and scientific advisory council. Gandy recently became associate director of the Alzheimer's Disease Research Center at Mount Sinai Medical Center in New York City.
The finding does have immediate relevance to the effort to develop treatments for Alzheimer's disease, Gandy said. "It reinforces the idea that anti-amyloid medication is a rational strategy," he said. "It reinforces the idea that attacking amyloid plaque helps nerve cells. You can see in nerve cells nearby changes in shape indicating that the cells are reacting to amyloid plaque, that is a link between those features of a pathology."
The study also answers a question about whether amyloid plaque can form only near blood vessels, Gandy said. "There have been reports that every amyloid plaque had a blood vessel somewhere," he explained. "That seems not to be the case."
But formation of amyloid plaque is not the only brain change associated with Alzheimer's disease, Hyman noted. Another notable feature consists of changes in the tau proteins that normally provide a scaffold for orderly function of nerve cells in the brain. Those tau proteins can become disordered, forming tangles that lead to destruction of nerve cells.
Studies of the formation of those tangles, using the same technology that led to the plaque discovery, are about to begin, Hyman said.
Keep up to date on Alzheimer's disease by consulting the Alzheimer's Association.
SOURCES: Bradley Hyman, M.D., Ph.D., director, Alzheimer's Unit, Massachusetts General Hospital, Boston; Sam Gandy, M.D., professor, Alzheimer's Disease Research, and associate director, Alzheimer's Disease Research Center, Mount Sinai Medical Center, New York City; Feb. 7, 2008, Nature
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