In setting out to explore the link between an immune system molecule and the amyloid plaques that characterize Alzheimer's Disease, a group of Yale researchers expected to find an inverse correlation between the two. That is, they assumed that more of the TGF-β protein would lead to less plaque build-up in the brains of mice engineered to develop Alzheimer's. Instead, the group found that by blocking TGF-β in these mice, they actually reduced the amount of the plaques, and even saw some improvement in the cognitive abilities of the mice.

The team of researchers, led by Dr. Terrence Town and working in the lab of Yale's Dept. of Immunology Chair Dr. Richard Flavell, found that in the group of mice with the TGF-β pathway blocked had as much as 90 percent less plaque buildup in their brains. The test mice performed better than mice with normal TGF-β fuctioning in maze navigation, which led the team to surmise that the neurocognitive processing had been improved with the blocking of TGF-β.

These animal results are very preliminary, but this new information does open up possiblities for new Alzheimer's research. “If results from our study in mice engineered to develop Alzheimer’s-like dementia are supported by studies in humans, we may be able to develop a drug that could be introduced into the bloodstream to cause peripheral immune cells to target the amyloid plaques,’’ said Terrence Town in a university release.

As Dr. Town points out, what this research indicates a new target for future exploration in Alzheimer's experimentation. While they have yet to be definitively linked to the cognitive declines seen in the disorder, amyloid plaques have long been thought to play some role in the cognitive deterioration of Alzheimer's. The plaques have been targeted by many previous studies, but the results have often been mixed or even disappointing. This new line of inquiry provides increased hope for success, and may even have set a new high bar since these mice did show cognitive improvements. It's a long way to go though from observing genetically engineered mice in a lab and seeing actual improvements with human adults in the real world, and many confounding factors could be found to be at work in mediating the symptoms that seemed to have improved in this study. Only further inquiry will bear out whether this line of research finally yields some traction on Alzheimer's or if scientists will have to head back to the drawing board.