"An experimental drug developed at Northwestern University has demonstrated further promise as an early intervention for Alzheimer's disease. In a new study published in Alzheimer's and Dementia: The Journal of the Alzheimer's Association, 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 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 experimental drug, a small-molecule compound called NU-9, decreased this toxic amyloid beta oligomer subtype 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 investigators are hopeful NU-9 potentially could prevent, or significantly delay, the cascade of toxic events that ultimately destroy neurons."
A previously unknown, highly toxic amyloid-beta oligomer subtype accumulates inside neurons and glial cells and initiates neuronal dysfunction, inflammation, and immune cell activation early in Alzheimer's pathogenesis. NU-9, a small-molecule compound, selectively reduced levels of this toxic oligomer subtype and markedly lowered associated neuronal damage in an Alzheimer's mouse model. Administering NU-9 before symptom onset prevented or significantly delayed downstream neurotoxic cascades that lead to neuron loss. Many clinical trials likely failed because interventions began after pathology was advanced; targeting oligomer accumulation in a presymptomatic window may improve therapeutic outcomes.
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