Mice study shows hallmark protein doesn't just clog circuitry, it gum ups the connections as well
THURSDAY, Sept. 19, 2013 (HealthDay News) -- A new study in mice offers more insight into the workings of the substance that clogs the brain's circuitry and appears to cause Alzheimer's disease.
Researchers now say they've found evidence that it doesn't just gum up nerve cells but also frays the connective wiring between them.
The scenario is the rough equivalent of gobs of glue clogging not only landline telephones but also the transmission lines that connect them.
The study is preliminary, and researchers have only examined mice so far. But the findings shed more light on the origins of Alzheimer's disease, suggesting that the fraying of the wiring happens early in the process, said study co-author Carla Shatz, a professor of biology and neurobiology at Stanford University and director of its BioX research program.
"It's really consistent with the idea that Alzheimer's begins earlier than you can diagnose it with imaging methods that look for the plaques and tangles in the brain," she said.
While physicians can try to treat symptoms like memory loss, Alzheimer's disease is incurable and often fatal. Researchers know that the beta-amyloid protein clumps into plaques that cause nerve cell death, which is a hallmark of the disease.
What the new research examined is how the protein sickens and kills the brain cells and how it disrupts the connections between them, Shatz said. "If we could understand the mechanisms for how all that happens, you could work on prevention or a cure," she noted.
The new study, published in the Sept. 20 issue of Science, reports that a form of the protein, called PirB, blocks the connection system in brain cells that handle transmissions between cells, she said. That sets in motion a process that destroys the synapses, the connections between nerve cells that are key to storing memories, processing thoughts and emotions and even helping the body to move.
So what can be done with this information? First, the research needs to be confirmed in people. Ideally, Shatz said, scientists would then come up with a medication that would prevent the cells in the transmission system from being gummed up. "It could be a new direction for research, but we're a long way from a drug," she said.
For now, physicians can only treat symptoms like memory loss but they can't stop the progression of Alzheimer's, which the Alzheimer's Association says is the sixth leading cause of death in the United States and will cost an estimated $203 billion in the nation this year.
Susan Landau, a research scientist with the Helen Wills Neuroscience Institute at the University of California at Berkeley, praised the research and said it's especially useful because it shows the beta-amyloid substance appears a decade or two before people develop signs of the disease.
"It would be particularly helpful if this mechanism made it possible to block the negative effects of amyloid well before the cognitive symptoms begin," she said.
For more about Alzheimer's disease, try the U.S. National Library of Medicine (http://www.nlm.nih.gov/medlineplus/alzheimersdisease.html ).
SOURCES: Carla Shatz, Ph.D., professor, biology and neurobiology, and director, BioX, Stanford University, Stanford, Calif.; Susan Landau, Ph.D., research scientist, Helen Wills Neuroscience Institute, University of California, Berkeley; Sept. 20, 2013, Science