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Could it make Alzheimer’s worse? Animal studies suggest that an antibody similar to one being trialled in people for the treatment of Alzheimer’s might actually be harmful.
Antibodies are currently undergoing trials in humans, as they have been found to break down the sticky plaques that build up in the brain. But in mice with a version of Alzheimer’s, antibodies that work the same way seem to make brain cells hyperactive and then eventually stop functioning.
“We think this is a possible mechanism for the failure of these antibodies in human trials,” says Marc Busche of the Technical University of Munich, Germany.
Busche and his colleagues gave an antibody drug to mice with Alzheimer’s-like disease and also to normal mice. After treatment, they found that mice with the disease had five times as many hyperactive brain cells than in treated normal mice.
Breaking up plaques
Alzheimer’s plaques form when protein pieces called beta amyloid clump together. Busche and his colleagues previously discovered that beta amyloid proteins can cause neurons to become hyperactive. They suggest that when the antibodies break up the plaques, it somehow aggravates this effect, making it worse than if the plaques remained intact.
In the wake of multiple failures trying to treat people with advanced Alzheimer’s disease, drug developers have switched to trying to detect and treat disease earlier.
So Busche and his team also studied the effect of the drug in mice with early-stage Alzheimer’s. Even in these mice, which had no plaques in their brains, neurons became hyperactive and symptoms of the disease worsened.
Mice can be misleading
“We find that even in very young mice, prior to plaque deposition, there’s an increase in hyperactivity,” says Busche. It’s not yet clear what process is causing the hyperactivity.
There’s no need to throw out these drugs just yet, though. Other researchers caution that mouse experiments have a
history of misleading results. “Mouse models are not perfect – we’ve been curing animals of Alzheimer’s for years,” says Maria Carrillo, chief scientific officer of the US charity Alzheimer’s Association.
Busche agrees that mouse models don’t mimic every aspect of human disease. “Treatments directed against amyloid beta are still promising,” he says, “but in the end we might need a combination of several approaches.”