Alzheimer’s drug: Scientists may have found a way to interrupt Alzheimer’s disease before symptoms emerge, based on tests of a new medication in laboratory animals.
Researchers at Northwestern University gave the experimental drug NU-9 to mice bred to develop Alzheimer’s-like conditions. The treatment sharply reduced concentrations of harmful protein fragments called amyloid beta oligomers, which clump together into the distinctive plaques found in Alzheimer’s patients’ brains.
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Mice receiving NU-9 showed far fewer oligomers in brain tissue. The drug also kept astrocytes, specialised brain cells that provide crucial support to neurons, from becoming overactive and inflamed. “These results are stunning,” said neurobiologist William Klein. “NU-9 had an outstanding effect on reactive astrogliosis, which is the essence of neuroinflammation and linked to the early stage of disease.”
Beyond testing the drug’s effects, the study aimed to map how Alzheimer’s begins years before patients notice any problems, knowledge that could reshape treatment approaches.
The research team identified a previously unknown variant of amyloid beta oligomer, which they labelled ACU193+. This subtype appears among the first to accumulate in stressed nerve cells, where it latches onto astrocytes.
Astrocytes normally help the brain function smoothly, but can turn destructive when excessively activated. The scientists suspect ACU193+ may trigger that harmful shift, potentially offering a target for intervention. “Alzheimer’s disease begins decades before its symptoms appear, with early events like toxic amyloid beta oligomers accumulating inside neurons and glial cells becoming reactive long before memory loss is apparent,” said Northwestern neuroscientist Daniel Kranz.
“By the time symptoms emerge, the underlying pathology is already advanced. This is likely a major reason many clinical trials have failed. They start far too late.”
Questions remain about whether amyloid beta, whether as oligomers or plaques, directly causes Alzheimer’s or simply accompanies it. Most experts believe multiple factors likely contribute to the disease.
Previous laboratory work showed NU-9 could prevent oligomer buildup in human brain cells grown in dishes. The new findings confirm that the drug also works in living organisms. Additional experiments are underway using animal models at later disease stages, which better mirror how Alzheimer’s progresses in ageing humans. Only after those tests could researchers consider moving to human trials.
If successful through all testing phases, NU-9 might eventually be given preventively to people at high genetic or lifestyle risk for Alzheimer’s, similar to how statins reduce heart disease risk by lowering cholesterol.
The findings appear in the journal Alzheimer’s & Dementia.