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Biological Chemistry

Boosting Immunity To Treat Alzheimer’s

Neuroscience: Inhibiting a protein that restrains immune responses leads to improved memory in mice

by Michael Torrice
January 25, 2016 | A version of this story appeared in Volume 94, Issue 4

A micrograph showing the brains of treated and untreated mice.
Credit: Nat. Med.
Mice injected with an antibody for PD-1 (right) had fewer amyloid-β plaques (red) in their hippocampus than those receiving another antibody (left).

A study in mice suggests that loosening the reins on the body’s immune system could help repair damage in the brain caused by Alzheimer’s disease. Inhibiting a protein that restrains immune responses cleared out characteristic protein plaques in the animals’ brains and improved their memory (Nat. Med. 2016, DOI: 10.1038/nm.4022). Michal Schwartz of Weizmann Institute of Science and colleagues last year showed that stimulating an immune response in mouse brains reversed symptoms of Alzheimer’s. They concluded that boosting immunity could be a strategy for treating the disease. In the new study, they looked for inspiration from cancer therapies that manipulate so-called immune checkpoint proteins to push the immune system to attack tumors. These signaling proteins encourage or discourage immune cells from springing into action. Schwartz’s team decided to test an antibody that inhibits PD-1, one of the checkpoint proteins. In mice genetically engineered to carry known Alzheimer’s mutations, the antibody led to recruitment of immune cells called macrophages to the brain. The mice later exhibited fewer plaques of amyloid-β—one peptide associated with the disease—and had improved performance in a test of learning and memory.


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