Neurogeneticists at the University of Southern California say that they were able to use immune cells to clear away amyloid beta, the toxic protein that may be the cause of Alzheimer's.
The team reports that they were able to spur the immune response by blocking interleukin-10, demonstrating the principle in a mouse study in which rodents displayed improved cognitive ability following treatment. Now they plan to take their work another step forward using genetically modified rats to create a model for the disease.
"Our study shows that 'rebalancing' the immune response to wipe away toxic plaques from the brain may bring new hope for a safe and effective treatment for this devastating illness of the mind," said Terrence Town, a professor of physiology and biophysics at the Keck School of Medicine of USC and the study's senior author.
Or not. There's no shortage of successful animal studies related to amyloid beta and Alzheimer's. But there is a clear shortage of clinical evidence that the amyloid beta approach actually works in humans. A series of late-stage failures has pointed more researchers down the path of early-stage disease work, theorizing that once the brain is damaged by toxic proteins reversing that damage may be beyond anyone's control.
Still, the rapid escalation of the disease among an aging population continues to drive preclinical studies like this one. And they'll continue until the biology of the disease is better understood.
Their work appears in the Feb. 4 edition of the peer-reviewed scientific journal Neuron.
- here's the release