New studies give insight into how Alzheimer’s spreads

Two new studies on mice have shown evidence that Alzheimer’s spreads from brain cell to brain cell like a virus, indicating the importance of early detection and treatment. But what is being spread is not a virus or bacteria, but a protein called tau. It is suspected that other brain diseases like Parkinson’s may spread the same way.

It has long been known that dying tau filled cells first appear in the small area of the brain that creates and stores memories. It then moves outward to the areas that deal with reasoning and remembering.

The studies, done independently by researchers at Harvard and Columbia University, used genetically modified mice that could make abnormal human tau proteins where the cells first start dying — the entorhinal cortex. As expected, tau showed up there and entorhinal cortex cells started dying.

Over the course of the two year study, cell destruction spread to other cells that could not make human tau — the only way they could get it was through transmission from cell to cell.

“This is a phenomenon that is increasingly recognized and potentially very important. If we understood this process, we could potentially arrest progression at an early stage,” said Dr. Samuel Gandy, of the Mount Sinai Alzheimer’s Disease Research Center in New York.

Researchers expect that, although the studies were done on mice, the same phenomenon happens in humans since the mice had a human tau gene and the cell death occurrence matched what is seen in Alzheimer’s patients.

Karen Duff and Dr. Scott Small of Columbia University Medical Center in New York worked on the study. “Everyone talks about Alzheimer’s ‘spreading’, but there really has not been a standard theory. In the past, we have asked many of our colleagues in the field of Alzheimer’s research what they mean when they say ‘spread’. Most think that the disease just pops up in different areas of the brain over time, not that the disease actively jumps from one area to the next. Our findings show for the first time that the latter might be true,” they told Reuters.

The mice also provide a tool to test ways to block tau’s spread, which could potentially bring Alzheimer’s to a halt.

“First, it would suggest that imaging tools that can detect entorhinal cortex dysfunction will be particularly helpful in diagnosing the earliest stages of the disease. More importantly, it might suggest ways of improving treatment. The implication of our study is that if it were possible to ‘treat’ Alzheimer’s when it was first detected in the entorhinal cortex, this would prevent spread,” said Duff and Small.

Current treatment focuses on amyloid, the protein that causes plaque to form in the brain. The scanners used can identify amyloid deposits, but not tau. Most late stage Alzheimer’s drugs target amyloid, which silently accumulates for 15 to 20 years before signs of the disease appear.

“Tau pathology might appear later in the disease but it is much more closely linked than amyloid to the time when people become demented, so intervening in tauopathy progression may be the better way to prevent or slow down dementia,” they noted. “For drug therapies, it is likely that targeting both amyloid and tau at the same time will be best.”

Sources: New York Times, Reuters

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