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Published on: June 27, 2012
by Janice Wood for Psych Central:
The spread of Alzheimer’s disease through the brain leaves dead neurons and forgotten thoughts in its wake. But researchers haven’t figured out how the disease spread.
Through experiments using stained neurons, a research team at Linköping University in Sweden has been able to demonstrate the process of neurons being invaded by diseased proteins that are then passed on to nearby cells.
“The spread of Alzheimer’s, which can be studied in the brains of diseased patients, always follows the same pattern. But until now, how and why this happens has not been understood,” says Martin Hallbeck, M.D., associate professor of pathology, who led the research team.
The disease starts in the entorhinal cortex — a part of the cerebral cortex — and then spreads to the hippocampus, two areas important for memory. Gradually, pathological changes take place in more and more areas of the brain, while the patient becomes even sicker, the researcher notes.
Two proteins have been identified in connection with Alzheimer’s: beta amyloid and tau. Tau is usually found in the axons — the outgrowths that connect between neurons — where it has a stabilizing function, while beta amyloid seems to have a role in the synapses where the neurons transfer signal substances to each other, Hallbeck said.
But in Alzheimer’s patients, something happens to these proteins, as autopsies reveal abnormal accumulations of both.
Why they become abnormal is still unknown, but what is known is that it’s not the large accumulations, or plaques, that damage the neurons, according to the researchers. Instead, smaller groups of beta amyloid — called oligomeres — seem to be the toxic form that gradually destroy the neurons and shrink the brain.
“We wanted to investigate whether these oligomeres can spread from neuron to neuron, something many researchers tried earlier but didn’t succeed,” Hallbeck said.
The study began with an experiment on neuron cultures, where researchers injected oligomeres stained with a phosphorescent red substance called TMR. The next day the neighboring, connected neurons were also red, which showed that the oligomeres had spread, according to the scientists.
To test whether a sick neuron can “infect” others, they conducted a round of experiments with mature human neurons stained green and mixed with others that were red after having taken up stained oligomeres. After a day, approximately half of the green cells had been in contact with a few of the red ones. After two more days, the axons had lost their shape and organelles in the cell nucleus had started to leak.
“Gradually more and more of the green cells became sick,” Hallbeck said. “Those that hadn’t taken up the oligomeres, on the other hand, weren’t affected.”
The researcher said that if a way of stopping the transfer can be found, it could lead to a more effective way to inhibit the disease.
The study was published in The Journal of Neuroscience.
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