“This drug is not a cure. It doesn’t stop people from getting worse, but it does measurably slow the progression of the disease,” said Dr. Joy Snider, a neurologist at Washington University in St. Louis. “That might mean someone could have an extra six months to a year of being able to drive.”

Randall Bateman of Washington University, St. Louis, presented the biomarker evidence, concluding that it indicates the treatment modified underlying biology. “These findings support the ability to change the course of Alzheimer’s disease,” he told Alzforum.

Biogen Inc. and Eisai Co. caused a stir in September when they announced positive results in a late-stage trial for a closely watched Alzheimer’s drug, lecanemab. Doctors tempered their excitement, though, until they could scrutinize the full peer-reviewed data.

That data arrived Tuesday night. And while it is stoking enthusiasm that physicians might soon be able to offer patients a treatment that can slow the progression of the devastating disease, doctors need to carefully balance that optimism with safety concerns and the reality that the drug is far from a cure — and in fact, it’s hard to quantify how meaningful it might be for a given patient.

The second (and third) time was not the charm for Roche’s experimental antibody drug for Alzheimer’s disease. The company last night announced gantenerumab had failed to show a statistically significant benefit in two large, late-stage clinical trials that tested its ability to slow patients’ cognitive decline—echoing a previous failure in another so-called phase 3 trial.

Researchers at Washington University School of Medicine in St. Louis have found an innovative way to improve waste clearance from the brain, and thereby possibly treat or even prevent neurodegenerative conditions. They showed that immune cells surrounding the brain influence how efficiently waste is swept out of the brain, and that such immune cells are impaired in old mice, and in people and mice with Alzheimer’s disease. Further, they found that treating old mice with an immune-stimulating compound rejuvenates immune cells and improves waste clearance from the brain.

Researchers at Washington University School of Medicine in St. Louis have found a new druggable pathway that potentially could be used to help prevent Alzheimer’s dementia.

A study by researchers at Washington University School of Medicine in St. Louis has shown that targeting astrocytes — an inflammatory cell in the brain — reduces tau-related brain damage and inflammation in mice.