The results of two new studies — both published in the journal Neuron — suggest that the brain’s immune cells may hold the key to future treatments for Alzheimer’s disease.
Your brain contains immune cells called microglia, which can be boosted to clear up Alzheimer’s-related brain damage, suggests new research.
Alzheimer’s disease affects more than 5 million people in the United States, and the condition ranks as the 6th leading cause of death in the country.
Among a range of other hallmarks, Alzheimer’s is characterized by neurological damage that is thought to be caused by plaques from a “sticky” protein called beta-amyloid.
Beta-amyloid is normally found in the membrane around nerve cells, but when it clumps together into small lumps or plaques between neurons, it can stop them from communicating with each other and impair brain function.
For years, researchers have been trying to understand exactly how the production of beta-amyloid triggers the symptoms of Alzheimer’s disease. Some researchers have even tried to develop anti-beta-amyloid drugs, but clinical trials of these pharmacological interventions have largely proven unsuccessful.
Now, researchers led by Prof. Huaxi Xu — the director of the Neuroscience Initiative at the Sanford Burnham Prebys Medical Research Institute in La Jolla, CA — offer a potential new strategy for eradicating the excessive buildup of the brain protein.
Prof. Xu and his team studied the behavior of a triggering receptor found on a type of cell called microglia — or the immune cells of the central nervous system — in two mouse studies. Their findings can be accessed here.
The receptor is called TREM2. As Prof. Xu explains, “Researchers have known that mutations in TREM2 significantly increase Alzheimer’s risk, indicating a fundamental role for this particular receptor in protecting the brain.”
But what the new research reveals is “specific details about how TREM2 works,” adds Prof. Xu. Specifically, the first study shows that amyloid beta binds to the receptor, triggering a chain reaction that may culminate with slowing down the progression of Alzheimer’s.
Once bound to the amyloid beta, the triggering receptor TREM2 then “tells” the immune cells to start breaking down and clearing out amyloid beta, “possibly slowing Alzheimer’s disease pathogenesis,” explains Prof. Xu.
The first study also demonstrates that TREM2 binds to so-called amyloid beta oligomers, which are molecular complexes that have been receiving more and more attention in specialist literature for their role in Alzheimer’s progression.
Also, the study showed that removing TREM2 in mice altogether interfered with the electrical currents that normally activate microglia.
The second study strengthened the findings of the first; it showed that “increasing TREM2 levels renders microglia more responsive and reduces Alzheimer’s disease symptoms,” says Prof. Xu.
More specifically, the researchers added TREM2 to mice that had been genetically modified to develop an aggressive form of Alzheimer’s.
More TREM2 signaling stopped the disease from advancing and even reversed some of the cognitive decline, the study authors report.
“These studies are important,” explains Prof. Xu, “because they show that in addition to rescuing the pathology associated with Alzheimer’s disease, we are able to reduce the behavioral deficits with TREM2.”
“To our knowledge,” he continues, “this provides convincing evidence that minimizing amyloid beta levels alleviates Alzheimer’s disease symptoms.” Prof. Xu also emphasizes that these findings offer a new therapeutic avenue.
“Going after microglia, rather than amyloid beta generation, may be a new research avenue for Alzheimer’s disease […] We could use brain immune cells to solve what’s becoming a public health crisis.”
However, he also cautions against potential pitfalls. “It could be beneficial in early stages to activate microglia to eat up amyloid beta […], but if you over-activate them, they may release an overabundance of cytokines (causing extensive inflammation) damaging healthy synaptic junctions as a side effect from over-activation.”
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