Experts say that a molecule released by special brain cells may open up entirely new treatment options in researchers’ ongoing fight against Alzheimer's disease.
Afflicting over six million people in the United States alone, Alzheimer’s disease has earned a troubling reputation as being one of the most common and dangerous forms of dementia known to the medical world. While most associate the disease with memory loss and other cognitive impairments, the science behind Alzheimer’s can help explain just how devastating the condition can be.
The mental decline linked with the disease occurs, in essence, once neurons and other cells in the brain begin to die. Once those neurons begin to die at an aggressive enough rate, the brain prepares a chemical response that, while evolutionarily designed to help, only sends the brain into a chemical spiral of which there is often no return.
But new research published Wednesday in the journal Nature suggests that experts have identified a specific molecule that may help the brain prevent this deadly spiral from ever taking place.
Researchers identified this potentially fateful molecule as interleukin-3, commonly known as IL-3. Originally discovered in mice and later humans in the 1960s, IL-3 is a protein that has historically been known to help the brain with stem cell management and the regeneration of platelets, but now experts believe that it may also have an important role to play in curbing the consequences of Alzheimer’s.
Experts say IL-3’s benefit to the brain boils down to one of Alzheimer’s most dangerous effects: neuroinflammation. Once enough neurons begin to perish in the brain due to Alzheimer’s, the brain activates cells known as microglia that begin to inflame entire regions of the brain in an effort to stop what the brain thinks is an infection that can’t be allowed to spread.
While this response is designed to help, the inflammation in fact only makes things much worse.
Rudolph Tanzi, co-director of the McCance Center for Brain Health at Massachusetts General Hospital, says neuroinflammation causes cells to die at a much faster rate than they otherwise would have and says that without this response, Alzheimer’s would look a lot different.
“As neuroinflammation ensues, the amount of cell death is at least 10 times higher than that which was caused by plaques and tangles,” Tanzi said. “In fact, without the induction of neuroinflammation, there would be no symptoms of dementia.”
Researchers say this is where IL-3 comes into play. Experts found that IL-3 is naturally programed to fight brain inflammation by turning microglia back into their more helpful forms. Once microglia are taught to stop causing the brain to inflame itself, they are redirected towards the task of cleaning up the original plaque deposits that are behind Alzheimer’s in the first place.
With the brain no longer at war with itself and its cells are busy fighting the correct targets, experts say the dangers of Alzheimer's become remarkable lessened.
“There may be important clinical implications to knowing that astrocytes talk to microglia via IL-3 to educate the microglia and help them decrease the severity of Alzheimer’s disease,” said Filip Swirski, who helped conduct the study while a principal investigator in the Center for Systems Biology at MGH.
“We can now think about how to use IL-3 to not only help curb the neuroinflammation that carries out the bulk of neuronal cell death in Alzheimer’s disease, but also to entice microglia to once again take on the beneficial task of clearing away the deposits and tangles that are the initiating pathology of Alzheimer’s disease.”
While researchers say they need to run more tests on how exactly IL-3 could be employed in neurological disease treatment options, they are nonetheless optimistic that this breakthrough could be the key to wining a major victory in the ongoing struggle against Alzheimer’s.Follow @@CarsonAndLloyd
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