Gonorrhea-Blocking Mutation also Protects against Alzheimer's: Study

Arthur T Knackerbracket has processed the following story:

According to the paper, a mutant form of an immune receptor, found in roughly one fifth of people, helps the immune system detect Neisseria gonorrhoeae, the bacteria responsible for the sexually transmitted disease. Typically, white blood cells particularly monocytes and macrophages, use a receptor called CD33, to distinguish between host cells and unwelcome pathogens invading the body. When CD33 binds to sialic acids-sugars that tend to adorn the membranes of host cells, acting as a molecular ID- immune cells recognize those cells and prevent the immune system from launching an attack.

But bacteria are expressing sialic acid as a way to fool the human immune system," Ajit Varki, a molecular biologist at the University of California, San Diego, who coauthored the study, tells The Scientist. To roam the body undetected, N. gonorrhoeae cover themselves in sialic acid molecules. When immune cells bind to the sugar coating, they misidentify the pathogen as a host cell, allowing it to go scot-free.

Our cells synthesize two forms of CD33: a full-length version and a mutated, inactive form that lacks the sugar-binding site. Those with a particular point mutation-different by a single changed nucleotide-produce a higher proportion of the mutant CD33, reducing the immune system's ability to recognize sialic acids. As a result, mutated immune cells are able to see through gonorrhea's disguise and initiate an attack. That same mutation, the researchers found, leads to a similar mechanism in the brain that protects neural tissue against Alzheimer's.

Just as the altered receptor helps the immune system target N. gonorrhoeae elsewhere in the body, it also helps the brain clear away damaged cells and amyloid plaques associated with Alzheimer's disease. Microglia-immune cells that patrol the brain-ignore the toxic amyloid build-ups when they interact with sialic acids. But this interaction is lost in individuals with the CD33 variant, allowing microglia to clear away amyloid aggregates.

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