Two recent studies published in January 2012 have found the path that Alzheimer’s disease seems to spread. Due to the results of these studies scientists now believe that Alzheimer’s spreads like an infection from brain cell to brain cell. However, instead of a virus or bacteria being spread, in Alzheimer’s brains a distorted protein known as tau is spread.
For a while scientists have know that dying tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to areas that involve remembering and reasoning. Alzheimer’s researchers have known that something sets off Alzheimer’s disease but have been unable to decide between two different explanations for the spread.
One of the theories is that the disease is transmitted from neuron to neuron, possibly along the paths that nerve cells use to communicate with one another. The other theory is that some of the brain areas are more resilient than others to the disease and are able to resist it longer.
For a while scientists suspected that a protein called beta amyloid was the most likely candidate for the spread, but they had never seen evidence that the amyloid spread from cell to cell in a network. Instead the amyloid creates a “bad neighborhood” in the memory regions of the brain. Tau, “the executioner” according to some researchers, comes into these bad neighborhoods and kills the cells. It was suspected that some cells take longer to succumb to the bad neighborhood, which would explain the spread of the disease. There would be no need to blame something odd like the spread of tau from cell to cell.
However, two studies that were done independently by researchers at Columbia and Harvard seem to provide proof that the other theory is correct. These studies involved genetically engineered mice that could make abnormal human tau proteins in the part of the brain where cells first start dying due to Alzheimer’s disease. Over the next two years, the cell death in the brains of the mice spread outward to other cells along the same network. These other cells could not make human tau so the only way they could get the protein was by transmission from nerve cell to nerve cell.
Even though these studies were done in mice, scientists expect that the same phenomenon occurs in humans since the mice had a human tau gene. The progressive wave of cell death also matched what is seen in people with Alzheimer’s disease. These new studies indicate that it may be possible to bring Alzheimer’s disease to stop by preventing cell-to-cell transmission of tau possibly with an antibody that blocks tau.
The use of the genetically engineered mice gives researchers a tool to test different ways to block the spread of tau in the brain. Some scientists believe that it may be necessary to not only block the tau, but also the beta amyloid production that seems to get the disease going. Regardless, these studies have led to an important discovery that could not only lead to a possible cure for Alzheimer’s disease, but also for other degenerative brain diseases may spread the same way.