Increased communication between brain cells increases levels of amyloid beta, the key ingredient in Alzheimer's brain plaques, scientists at Washington University School of Medicine in St. Louis have found.
The findings showed that turning up brain cell firing rates drove up levels of amyloid beta in the spaces between brain cells. Corresponding drops in amyloid beta levels occurred when brain cells' ability to send messages was dampened or blocked completely.
The results, produced in mouse models of Alzheimer's, will appear in the journal Neuron on Dec. 22. They complement a Washington University study published earlier this year that used functional brain imaging to show that the brain areas that develop Alzheimer's plaques are also the regions that are the most active in healthy young people who are daydreaming or not carrying out a specific cognitive task (http://news-info.wustl.edu/news/page/normal/5621.html).
The two papers have researchers considering the possibility of someday slowing or preventing the development of Alzheimer's disease by using pharmaceuticals to selectively reduce some communication between brain cells. However, researchers still have to determine if increased levels of amyloid beta can be partially linked to particular classes of the nerve cell messengers and receptors that cells use to communicate with each other.
"Ideally, we will be hoping to find a drug or mechanism that could very specifically target the processes that lead to increased amyloid beta levels," says lead author John Cirrito, Ph.D., a postdoctoral research associate in neurology and psychology. "If we can identify these and find ways to modulate them, we'd have new ways of intervening in Alzheimer's disease."
Senior author David Holtzman, M.D., the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology, says that the results do not contradict earlier studies that suggested crossword puzzles, exercise and other mental stimulation can reduce the chances of developing Alzheimer's disease.
According to Holtzman, their new results and the WUSTL study published earlier this year instead offer further evidence that "cognitive idleness is not good from the perspective of Alzheimer's risk." The lead author of the earlier study, published in The Journal of Neuroscience, was Randy Buckner, Ph.D., associate professor of psychology at the School of Arts and Sciences and associate professor of neurobiology and radiology at the School of Medicine.
Together, these two studies may provide an explanation why specific regions are vulnerable to this disease. Holtzman and Cirrito speculate that activities such as crosswords and exercise may increase activity in brain areas less likely to be damaged by Alzheimer's and cause a corresponding reduction in activity levels in the regions consistently damaged by Alzheimer's disease.
"Almost all neurological diseases involve selective vulnerability--only certain classes of nerve cells or nerve cells found in particular regions are affected," Holtzman says. "Why that vulnerability is so selective often can be very difficult to determine, and Alzheimer's disease is no exception."