While you might associate protein mainly with packing on muscle and getting ripped, different types of proteins do all kinds of positive jobs in the body–they can transport atoms and molecules through you, work as antibodies, transmit signals and carry out thousands of cellular chemical reactions, for starters. But new research suggests that one protein might be playing the villainous Joker, stealing away brain health, speeding functional decline and upping the odds you develop Alzheimer’s.
The study, as explained by Alzheimer’s researcher Tony Wyss-Coray of Stanford University, used mice to focused on the Vascular Cell Adhesion Molecule 1 (VCAM1) protein, which is found in the cells that form the blood-brain barrier. The purpose of the barrier is to protect you from any harmful agents in your blood, and the VCAM1 protein interacts with immune cells when inflammation occurs.
Scientists know that, as you age, the amount of VCAM1 found in your blood increases. But Wyss-Corey and his team wanted to understand more clearly how this affected the brain. They thus injected young mice behind the eye with plasma from old mice. Levels of VCAM1 in the blood-brain barrier went up in specific parts of the blood-brain barrier in the injected mice. Wyss-Corey also saw that the injected mice suffered inflammation, brain deterioration and a lowered number of new nerve cells. These effects weren’t present when Wyss-Corey injected plasma from young mice.
Treatment options to come
With the research clearly indicating that VCAM1 could be problematic, the next logical question of course then is, how in the world can you put the brakes on it and protect your brain? Wyss-Corey explored a little further. He injected VCAM1 again, this time using mice that had been genetically engineered to lack VCAM1 in particular blood-brain barrier cells. He also injected VCAM1 into mice that had been given antibodies that block VCAM1 activity. In both cases, the negative effects initially noted didn’t happen. What’s more, mice that aged naturally and that received VCAM1 antibody treatment showed slowed signs of brain deterioration, too. This suggests that both gene and antibody therapies could be potential routes for doctors to keep the brain young and healthy.
This is only the start
Wyss-Corey and his team saw good results, but the study is preliminary. And significantly, mice aren’t people. Researchers have to do more work to see if they can replicate the results in humans. And even if that’s successful, there’s still the job of standardizing specific gene and antibody therapies that regulatory agencies such as the Food and Drug Administration will approve. So this isn’t something we’re going to fix by tomorrow. Still, the path seems to have had its cornerstones laid. Considering that the number of Americans living with Alzheimer’s is predicted to reach 16 million by 2050, and accepting more generally how essential brain health is to quality of life and business ferocity, that’s very good news.