Alzheimer’s disease has long been regarded as irreversible, but new scientific research has challenged that notion.
A study at Northwestern University in the US has shown that an experimental drug can halt . and even reverse – early brain damage linked to the disease, rather than simply slowing its progression.
Working with mice, the research team identified a previously unrecognised subtype of highly toxic protein oligomers believed to trigger the earliest stages of the disease.
These proteins appear to drive initial brain changes such as neuronal dysfunction, inflammation and the activation of immune cells.
‘We identified a distinct subtype of beta-amyloid oligomer that forms inside neurons and may act as a key instigator of early Alzheimer’s pathology,’ explained Daniel Kranz, one of the study’s authors.
The experimental drug, known as NU-9, was shown to significantly reduce these toxic molecules, dramatically limiting the damage they cause in the brain.
Researchers stress that Alzheimer’s begins decades before memory loss becomes apparent, with harmful biological processes already underway long before diagnosis.
‘When symptoms emerge, the underlying disease is already advanced,’ said Kranz.
‘This is likely why so many clinical trials have failed – treatment starts too late. In our study, we administered NU-9 before symptoms appeared, modelling a critical early window where intervention may be most effective.’
In the trial, pre-symptomatic Alzheimer’s mice received a daily oral dose of NU-9 for 60 days. The results were striking.
The drug significantly reduced early reactive astrogliosis, an inflammatory response that usually appears well before clinical symptoms.
Levels of toxic oligomers also fell sharply, along with abnormal forms of the protein TDP-43, which is commonly linked to neurodegenerative diseases and cognitive decline.
Improvements were observed across multiple brain regions, suggesting NU-9 produces a brain-wide anti-inflammatory effect.
One of the researchers, Richard Silverman, compared the potential use of NU-9 to cholesterol-lowering medication.
‘People monitor cholesterol to prevent future heart attacks,’ he explained. ‘If someone shows biomarkers indicating Alzheimer’s risk, NU-9 could be taken in the same preventive way, before symptoms ever appear.’
This approach is becoming increasingly realistic as blood-based tests for early Alzheimer’s detection continue to advance.
Researchers believe that combining early diagnosis with preventive treatment could fundamentally change how the disease is managed.
The team is now testing NU-9 in additional Alzheimer’s models, including a late-onset version that more closely mirrors typical human ageing.
They also plan long-term studies to determine whether early treatment prevents the development of symptoms and preserves memory and brain health over time.
Despite the encouraging findings, the researchers caution that human clinical trials will be essential.
‘This new therapeutic strategy must now be tested in carefully designed trials to determine whether the benefits seen in animals can be replicated in people,’ the study concludes.
