Scientists have identified a new therapy for Alzheimer’s—one that could potentially treat the disease at any stage. It may even be applicable to other neurodegenerative diseases, if clinical trials for the drug are successful.
Alzheimer’s disease is characterized, in part, by a weakened immune system. That hindered response could be preventing the body from healing itself, suggested Michal Schwartz of the Weizmann Institute of Science in Rehovot, Israel. Schwartz and her colleagues havepublished a study in the journal Nature Medicine detailing this effect and illustrating the promise of immunotherapy drugs known as PD-1 blockers in preventing Alzheimer’s patients’ immune systems from shutting down.
The researchers used mice to demonstrate that PD-1 blockers slash the amount of sticky amyloid beta—a plaque thought to have a role in causing Alzheimer’s—in half. And when they sent the mice through a maze after receiving the PD-1 injection, their cognitive abilities improved.
Here’s Sarah Knapton, reporting for The Telegraph:
In cancer the drugs work by disabling an “immune checkpoint” called the programmed cell death receptor 1, or PD-1, which stops immune cells from attacking tumors. These checkpoints are designed to prevent the immune system killing healthy cells but they are exploited by cancer to avoid detection.
The finding is particularly interesting because previously scientists believe that an over active immune system could be responsible for Alzheimer’s and were puzzled why anti-inflammatories did not see to have any impact in trials. The new research suggests the opposite could be true.
Schwartz and her team believe that boosting the brain’s immune system could help it purge toxic substances like amyloid beta and Tau protein “tangles,” which also appear to accumulate in the brains of Alzheimer’s victims.
When under siege by amyloid beta and Tau proteins, the brain triggers an inflammatory response that theoretically should be helpful. In recent years, though, scientists have argued that inflammation becomes harmful after a certain point. But attempts to calm the brain’s microglia (immune cells) have been met with mixed results—making the role of inflammation in neurodegenerative disease all the more unclear. Still, several immune system genes, such as APOE e4 and IL1RAP, have been associated with plaque build-up—meaning that the immune system has a critical place in Alzheimer’s research. We just haven’t found the best point of focus yet.
Because they target the overall immune system, though, Schwartz’s finding suggests that PD-1 blockers may be appropriately used at various stages of the disease’s progression. Moreover, the U.K. and the U.S. have already approved the PD-1 blocker Keytruda for use in treating advanced melanoma and advanced non-small cell lung cancer. Given these recent developments, Keytruda may become a key player in the push to understand immunotherapy and Alzheimer’s disease.