Alzheimer's Disease Spreads Like a Virus? Not So Fast

“Alzheimer’s disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau. ...” So began an article in the research section of the Feb. 2 issue of The New York Times. The article went on to say that this “surprising finding … has immediate implications for developing treatments.”

But the finding was the result of studies in mice. Can we really make the leap from mice to men (and women) “immediately”? Or even quickly? “No,” says Dr. Ralph Nixon, director of the Silverstein Institute on Brain Aging at New York University's Langone Medical Center, who was not involved in either study. “I don't see any immediate implications for treatment development or any immediate treatments stemming from these findings in a mouse model. A lot more research needs to be done to understand the implications and what treatments might emanate from them.”

Simply put, the article posits that Alzheimer’s and possibly other degenerative diseases damage the brain by spreading a protein, tau, from nerve cell to nerve cell. Tau is part of the scaffolding that supports and protects the brain's nerve cells. High levels of tau have been linked to poor recovery from brain trauma and abnormal tau forms clumps, called “tangles,” that are considered a marker of some forms of dementia, including Alzheimer's disease. But tau has not been proven to cause Alzheimer’s or dementia. Nevertheless, the Times article states that “it may be possible to bring Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau.”

By comparing the spread of tau from nerve cell to nerve cell to a virus, “the reporter made an unfortunate, highly speculative analogy that could be very disconcerting to the average reader by casting this as though Alzheimer's were an infectious disease,” Nixon says. “The journal articles are much more cautious in their interpretations.” (John Hardy of University College London, who comments in the Times article that degenerative disease development involves “… contagion from one neuron to another,” was not involved in either study).

As Nixon explains: “Molecules pass from one neuron to another during the normal functioning of the brain. You can’t make the leap that if you put a large amount of the protein in one neuron and then you see the presence of that protein in another neuron, that there’s a viral-like passage of that protein. There could be many other reasons for that.”

If, despite all the caveats, we still went with the idea that Alzheimer’s somehow spread from cell, even Hardy acknowledges that “it may be necessary to block both beta amyloid production, which seems to get the disease going, and the spread of tau, which continues it, to bring Alzheimer’s to a halt” — hardly an undertaking that could yield speedy results, unfortunately.

What's potentially important about these new studies and others like them is that they could ultimately provide valuable information on the progression of Alzheimer's and other dementias. However, it is vital that they be viewed in the proper context and correctly interpreted. This whole scenario points to the need to carefully assess stories about research findings — no matter where they appear — and particularly if they hint at a quick cure to longstanding, devastating chronic diseases that generally are caused by an interplay of genetic, environmental and behavioral factors.