Skip to content

Might immune response to viral infections slow birth of new nerve cells in brain?

Another reason to keep a cool head, at least if you're a mouse: this study, just published in the Journal of Neuroscience by Tony Wyss-Coray, PhD, and his Stanford colleagues. Inflammation may not a healthy brain make.

A protein that goes by the name C3 is central to shaking awake our bodies' immune cells so they more quickly perform their jobs such as repairing damaged tissue or gobbling up bad actors in the blood or tissue. Large amounts of C3 are always present in our blood, with no immediate consequence.

But inflammation - our primary response to injury and invasion - causes this protein to get hacked to pieces. Immune cells - carry several several different receptors in their surfaces for the various different fragments of C3 that are created in the "Wake Me, Shake Me" process.

As it happens, one of these receptors, called CR2, also shows up on brand-new brain cells: specifically, the so-called neural progenitor cells that generate new nerve cells that help that all-important brain structure, the hippocampus, consolidate short-term into long-term memory.

When Wyss-Coray and his colleagues experimentally loaded up mice's brains with high levels of the particular C3 fragment that binds to CR2, new nerve-cell production in those mice's hippocampus plummeted. In mice specially bioengineered so that CR2 (the receptor) was absent, new nerve-cell production was significantly increased in comparison with normal mice.

Intriguingly, introduction of alpha-interferon - a naturally occurring antiviral protein the body produces under inflammatory conditions such a a viral infection - led to diminished new nerve-cell generation in mice. Maybe that's not so great, because the genetically engineered version of alpha-interferon is a recognized treatment for patients with certain cancers or viral infections such as hepatitis C. More than one-third of such patients have been reported to develop depression or cognitive deficits linked to the treatment, and normal function is regained after treatment is discontinued.

Kind of gets you wondering whether inflammation - in response to infection, or as a chronic condition of aging - might play a role in neurodegenerative disease, doesn't it? And say, have you popped your daily NSAID?

Popular posts