The cells in your immune system eat 100 billion dead cells in your body every day.
But sometimes, your body eats living cells, too — even though it’s not supposed to. Scientists don’t know why, but a new study from a team at the Salk Institute says that cellular barbarism might be the key to treating a host of neurodegenerative diseases.
Most people think by the time you’re an adult, you’re done making new neurons. But some parts of your brain are molecular busybodies and want to keep making them, so you end up with a lot more neurons than you need, and they end up dying.
To keep the neurons in check and not turn your body into a big neural graveyard, your immune system uses what are called microglia to clean out the dead neurons. Microglia are pretty much the trash collectors of your central nervous system. Unlike synaptic pruning, which just nibbles off the connections between neurons, this process — called phagocytosis — involves eating entire cells.
In order for the microglia to know which cells to kill, they need to have TAM receptors: the bouncers to the club in your body that decides which cells can stay.
Two of those receptors are called Axl and Mer — TAM’s “A” and “M,” respectively. To clear the cells, your body needs Axl and Mer. If a microglia doesn’t have those, the dead neurons won’t clear, and now you’re full of billions of dead neurons.
Mer is naturally involved in phagocytosis in the brain — if that’s happening, it means everything is in order.
“Mer is what we call the ‘steady as she goes’ receptor,” Greg Lemke, lead on the study and a professor of molecular neurobiology at the Salk Institute, said in a phone interview Tuesday. “The other one, Axl, is turned on when there’s a stimulus.”
Stimulus, in this case, means infection. Or trauma. Or a neurodegenerative disease linked to inflammation, like Parkinson’s disease.
But it’s good for researchers: The stimulus “has turned out to be a general marker of inflammation,” Lemke said. “We’re excited about its potential use as a marker for the level of disease activity in the degenerative brain.”
This means if something’s going wrong in your brain, doctors can check those Axl levels. If the levels are high, it probably means something’s screwed up.
In the five-year period Lemke’s team studied the TAM receptor levels, elevated levels of Axl were the single best predictor of the speed with which Alzheimer’s disease progressed in mice.
Here’s where it gets good. When you inhibit Axl and Mer, you block the process of clearing out dead or dying cells. Even though dying, sick cells sound like a bad thing to have in your body, getting rid of all of them could actually be dangerous to people with brain disease.
“We found that, if you don’t have Axl and Mer in the mouse model, you slightly extend the lifespan of those mice,” Lemke said. Inhibiting Axl has also been linked to fighting various types of cancer, including lung, ovarian, colorectal and melanoma.
Elevated levels of Axl were the single best predictor of the speed with which Alzheimer’s disease progressed in patients.
Since TAM receptors are active in both the body and the brain, Lemke’s lab reasoned that the same inhibiting approach to cancer might also be able to work on degenerative diseases.
“Companies are trying to develop inhibitors of these TAM receptors all the time — it’s the basis for many cancer therapies,” Lemke said.
There’s still a lot of work to do, Lemke admitted. He doesn’t know why microglia eat living cells, like some predator tracking the weakest of your body’s flock. He doesn’t know if targeting Axl and Mer could work for brain diseases the way it works for cancers. And he doesn’t know if the results he found in the mouse models will work the same way with human brain structures.
But if Lemke is right, this research could mean knocking brain disease to the dirt.
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