In 1907, the German psychiatrist Alois Alzheimer published a description of a 50-year-old woman who suffered from memory problems, hallucinations, and delusions. In the woman’s brain, Alzheimer noticed unusual lumps, or “plaques,” which “were caused by the deposition of an unusual substance.” Eight decades later, the mystery substance was finally identified as a protein called amyloid beta. Though small, it can accumulate in large clusters that are somehow toxic to neurons. Those harmful plaques are one of the hallmarks of the disease that bears Alzheimer’s name.
What amyloid beta normally does in the brain isn’t clear. Robert Moir, a neurologist at the MassGeneral Institute for Neurodegenerative Disease, says that many researchers have cast it as a villainous molecule with no beneficial function. “It’s just bad, bad, bad,” he says. “But it has become increasingly obvious that this isn’t true.” Moir thinks that amyloid beta has a more heroic role, as a foot soldier of our immune system. It protects neurons from infectious microbes—and from herpes viruses, in particular.
William Elmer, a member of Moir’s team, demonstrated this protection by injecting the common herpes virus HSV–1 into the brains of two kinds of mice: normal rodents and ones that were genetically engineered to produce high levels of amyloid beta in their brains. The latter were better at resisting the viruses. Elmer then got similar results when he injected a different herpes virus, HHV–6, into human cells growing in a dish.
Amyloid beta protects against these viruses by latching onto them in large numbers, imprisoning them in self-assembling cages. That’s typically a good thing, but Moir argues that if the process goes on for too long, it builds up to the problematic plaques of Alzheimer’s. According to him, amyloid beta is still at the heart of the Alzheimer’s story, but it …read more
Source:: The Atlantic – Health