If you have ever seen a wildfire you know it is hard to stop, and fuels smaller fires from the sparks flying through the air, making it hard to control. It destroys everything in its path. This is what happens once our brains have been invaded with memory loss. The neurons (brain cells) that are affected communicate with other neurons until the cells no longer have any spark.

According to a new study, a distorted protein known as “tau” causes this wildfire. A dying, tau-filled cell first begins in a small area of the brain where memories are stored. The disease then spreads outward, moving slowly to larger areas of the brain involving reasoning and memory.

The new study provides some answers to questions neuroscientists have been trying to understand for more than a quarter-century. Up until now they didn’t know if the disease is transmitted from neuron to neuron through synapse, or that some cells are prone to this protein while others are resistant. The study indicates it may be possible to abruptly halt the progression of Alzheimer’s disease by preventing cell-to-cell transmission, if an antibody that blocks the tau protein.

The independent study, conducted by researchers at Columbia and Harvard, used genetically engineered mice that could produce abnormal human tau proteins, mostly in the entorhinal cortex, a sliver of tissue behind the ears and toward the middle of the brain where cells start to die first in Alzheimer’s patients. As the researchers expected, tau was found there, and the entorhinal cortex cells in the mice began to die were filled with the tangled, spaghetti-like strands of tau.

The progression of the cell death over the next two years spread outward to other cells along the same network. Because the other cells could not produce the human tau, the only way they could get the distorted tau protein was by transmission from nerve cells to nerve cells.

Even though the studies were conducted with mice, researchers believe they will find the same phenomenon in humans because the mice had a human tau gene, and the progressive wave of cell death matched what they see in people with Alzheimer’s disease.

Two separate studies, one conducted by Karen Duff and Dr. Scott A. Small and their colleagues at the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center, was published in the journal PLoS One. The other, by Dr. Bradley T. Hyman, director of the Alzheimer’s Disease Research Center at Massachusetts General Hospital, and his colleagues, was published in the journal Neuron.

Both groups of researchers were given the inspiration from the many observations over the years that Alzheimer’s begins in the entorhinal cortex and spreads.  But, said Dr. Small, “what do we mean by ‘spreads?’”

The solution came when researchers were able to develop genetically engineered mice that expressed abnormal human tau, but only in their entorhinal cortexes. Those mice offered the cleanest way to get an answer, said John Hardy, an Alzheimer’s researcher at University College London who was not involved in either of the new studies.

There is another advantage, too, Dr. Hyman said. The mice give him a tool to test ways to block tau’s spread — and that, he added, “is one of the things we’re excited about.”

But if tau spreads from neuron to neuron, Dr. Hardy said, it may be necessary to block both beta amyloid production, which seems to get the disease going, and the spread of tau, which continues to bring Alzheimer’s to a halt.

He and others are also asking if other degenerative diseases spread through the brain because proteins pass from nerve cell to nerve cell, such as Parkinson’s disease.



About the author:

Ron White is a two-time U.S.A. Memory Champion



NY Times – Path is Found for Spread of Alzheimer’s: http://www.nytimes.com/2012/02/02/health/research/alzheimers-spreads-like-a-virus-in-the-brain-studies-find.html?ref=research