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Alzheimer’s Research Update

October 8, 2009
According to researchers at?UT Southwestern Medical Center, the negative action of beta-amyloid, the protein involved in Alzheimer’s disease, can be counterbalanced with another brain protein, called Reelin. Beta-amyloid’s normal function is like a red traffic light, restraining nerve cells from getting overexcited when they receive stimulating signals from neighboring cells. People with Alzheimer’s disease, however, accumulate too much beta-amyloid — the traffic light gets stuck on “red” and nerve cells become less responsive. Reelin acts like a green light, stimulating nerve cells to respond more strongly to their neighbors’ signals.?This study, done with mice, shows that applying Reelin directly to brain slices 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.?The experiments showed 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.?This mechanism also includes another protein involved in Alzheimer’s, ApoE4, which is the primary risk factor for the most frequent late-onset form of AD. 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,” Dr. Herz said. “This study establishes a rationale that ApoE receptors have an action that can keep the Alzheimer’s disease process at bay by preventing damage in the first place.”?Mimicking or preserving normal Reelin function to stimulate the ApoE receptors might provide a path to stave off the disease, Dr. Herz said.?