A new approach to treat Alzheimer's disease has been advocated by researchers at UT Southwestern Medical Centre.
They suggest that the action of a small protein that is a major villain in Alzheimer's disease can be counterbalanced with another brain protein.
The harmful protein, called beta-amyloid, is found in the brain and, when functioning properly, suppresses nerve activity involved with memory and learning.
Its normal function can be likened to a red traffic light, restraining nerve cells from getting overexcited when they receive stimulating signals from neighbouring cells.
Another brain protein, called Reelin, acts as a "green light," stimulating nerve cells to respond more strongly to their neighbours' signals.
The study showed that applying Reelin directly to brain slices from mice prevents excess beta-amyloid from completely silencing nerves.
"If we can identify a mechanism to keep the nerve cells functioning strongly, that might provide a way to fight Alzheimer's disease," said Dr. Joachim Herz, professor of molecular genetics and neuroscience at UT Southwestern and the study's senior author.
In the study conducted using mouse model, the researchers determined that Reelin and beta-amyloid interact with the same protein complex, called an NMDA receptor, which plays an important role in coordinating chemical signals between adjacent nerve cells.
They found that Reelin activates and strengthens the response of the NMDA receptor.
In the presence of too much beta-amyloid, the receptor migrates into the cell, reducing the cell's sensitivity to incoming signals. By contrast, in strong concentrations of Reelin, the receptor remains active and the cell has the green light to continue receiving normally.
Dr. Herz said the study is especially important because this mechanism involves another protein involved in Alzheimer's called ApoE4, which is the primary risk factor for the most frequent late-onset form of the disease.
The receptor that binds to ApeE molecules also binds to Reelin, and is part of the red-light/green-light complex that controls the sensitivity of the NMDA receptors.
"These results imply that Reelin, ApoE and beta-amyloid converge on the same molecular mechanism, which is critical in the Alzheimer's disease process, and Reelin may be a common factor to fight both beta-amyloid and mutated ApoE," Herz added.