Tau Proteins Spread More Easily in Aging Brains, Finds Study .

Massachusetts General Hospital, Boston

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By Jacqueline Ahearn | July 12th, 2019

While not every elderly person develops Alzheimer’s, age is a risk factor for the disease. Currently, one in 10 people over the age of 65 are living with Alzheimer’s disease. For years, researchers have been studying the link between old age and Alzheimer’s to determine what makes an aging brain more susceptible to this form of dementia.

Now researchers have uncovered a possible connection. The new study, published in the journal Science Advances, found that tau proteins, a hallmark of the disease, spread more easily in aging brains.

Alzheimer’s research has largely focused on two kinds of protein deposits in patients’ brains: amyloid beta plaques and tau neurofibrillary tangles.

How Tau Tangles May Impact Alzheimer’s Symptoms

Many researchers believe that when tau protein tangles accumulate in the brain, it leads to Alzheimer’s symptoms. Tau tangles begin in the brain’s memory centers and then show up in other areas of the brain as the disease progresses. That, they theorize, is why Alzheimer’s begins with memory problems and then eventually leads to difficulty with daily functioning.

While researchers have also been investigating the role of beta-amyloid plaques — another toxic protein associated with Alzheimer’s — several have turned their attention to tau, after drug trials targeting beta-amyloid have continued to fail.

As targeting beta-amyloid consistently fails to produce the desired results, researchers have accordingly changed their analysis. Although it is still unclear the extent to which beta-amyloid may play a role in the development of Alzheimer’s, it is becoming increasingly clear that tau proteins may be a larger factor in halting the disease’s progression.

How Tau Proteins Spread in the Aging Brain

To study the development and spread of tau neurofibrillary tangles over time, the researchers used a tailored virus particle called a gene vector to channel the blueprint of the human tau protein into the brains of mice.

Over the course of 12 weeks, they examined how far the tau tangles had spread in the mice. “Human tau proteins spread about twice as fast in older mice as compared to younger animals,” explained head researcher Susanne Wegmann, PhD, of the German Center for Neurodegenerative Diseases (DZNE) in Berlin, Germany.

In layman’s terms, the increased spread of the protein in aging brains makes people more susceptible to Alzheimer’s over time. The study also found that tau is produced by young, healthy brains and can convert to a toxic version of the protein, which is prone to tangles. This suggests that not only is an accumulation of defective tau a risk factor, but even an accumulation of healthy, normal tau may increase the risk of developing Alzheimer’s.

The study raises additional questions, which Wegmann and her team intend to tackle in future studies, such as, Is too much tau protein produced or too little defective protein removed? Also, which processes underlie the increased spreading of tau in the aging brain?

An unrelated study this past week found that a brain molecule called VPS35 clears defective tau tangles in the brain, but doesn’t work as well in people with Alzheimer’s disease.

Clearly, more research is needed to connect the dots. However, this study is the first step to answering these questions, which may unlock future therapeutic treatments for those with Alzheimer’s. The study was carried out in close collaboration with researchers in the U.S. at Harvard Medical School and Massachusetts General Hospital.