A new drug could stop Alzheimer’s before memory loss begins

New research suggests Alzheimer’s may start far earlier than previously thought, driven by a hidden toxic protein in the brain. Scientists found that an experimental drug, NU-9, blocks this early damage in mice and reduces inflammation linked to disease progression. The treatment was given before symptoms appeared, targeting the disease at its earliest stage. Researchers say this approach could reshape how Alzheimer’s is prevented and treated.

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An experimental drug developed at Northwestern University has demonstrated further promise as an early intervention for Alzheimer's disease.

In a new study, Northwestern scientists identified a previously unknown highly toxic sub-species of amyloid beta oligomers -- toxic clusters of peptides -- that appear to drive several of the brain's earliest changes, including neuronal dysfunction, inflammation and activation of immune cells.

The experimental drug, a small-molecule compound called NU-9, decreased this toxic amyloid beta oligomersubtype and dramatically reduced the damage it causes in a mouse model of Alzheimer's disease. By addressing these changes at the onset of Alzheimer's disease, the researchers are hopeful NU-9 potentially could prevent, or significantly delay, the cascade of toxic events that ultimately destroy neurons.

The findings point to a potential new strategy for targeting the disease in its earliest stages -- before cognitive decline and other debilitating symptoms take hold.

The study will be published on Dec. 18 in Alzheimer's and Dementia: The Journal of the Alzheimer's Association.