Even when the body has reached the peak of development, there are certain regions of the brain where neurons continue to grow. In order to keep these areas neat and clean, the brain recruits immune cells uniquely designed to clear out the dead and dying cells in the brain.
Acting as a “garbage collector” is not a new function to the body’s immune cells or to the scientists studying them. Throughout the body, macrophages are pushed by two TAM receptors, Mer and Axl, to clear out the “junk” cells that get in the way. Immune cells express Mer and Axl to get the job done.
However, in a new study from the Salk Institute, published in Nature
, scientists are just now realizing the “surprising extent” to which specific cellular switches are controlling a similar “garbage collection” in the brain. Microglia act just like macrophages except strictly in the central nervous system, and these cells make up ten percent of all brain cells.
Healthy microglial function is important for both regular maintenance of brain health and for repair during a state of damage. Inspired by the potential for learning more about treating neurodegenerative diseases and inflammatory diseases like Parkinson’s, scientists from the current study began mice studies to pinpoint just how Mer and Axl instigate regular trash pick-up.
When Mer and Axl were experimentally removed from mice microglial populations, scientists saw a large aggregation of dead cells, but only in areas where neurogenesis occurs. Additionally, the amount of new neuron migration to the olfactory bulb largely increased when Mer and Axl were missing.
In mice lacking the TAM gene altogether, scientists saw a 70 percent increase of new neurons in the olfactory bulb. Scientists are still unsure how, if at all, this type of mutation would impact a mouse’s sense of smell.
In addition to appearing to affect neuronal migratory tendencies, Mer and Axl seemed to be playing another role, the scientists thought. Prompted by these two TAM receptors, microglia target healthy cells in addition to the dead and damaged. Although this seems detrimental to brain health, for a normal brain this is a beneficial function, because extra cells are usually not necessary for healthy brain function. However, if a brain is anything less than healthy, as in cases of Parkinson’s disease for example, deleting any extra healthy cells would certainly make the condition worse.
In mice models of Parkinson’s disease, deleting Axl and Mer actually helped mice live longer, with Axl being indicative of tissue inflammation in cases of neurodegeneration. This discovery has scientists realizing that these TAM receptors are in fact making diseases like Parkinson’s progress faster because they are killing too many cells.
From this discovery, it seems that the scientists from the Salk Institute are on the brink of developing a new treatment plan for neurodegenerative and inflammatory brain diseases. However, instead of inserting something that the body is lacking for healing, scientists will inhibiting a self-inflicting mechanism to treat the condition.
Source: Salk Institute