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Getting the latest healthcare news for you
Getting the latest healthcare news for you
Decades of research may unlock earlier Alzheimer's treatment. At AAIC 2026, neurologist Takaomi Saido, PhD, presented findings on neprilysin — a key enzyme that breaks down amyloid-beta — and its potential as a therapeutic target before symptoms even begin. His team is also working to identify the molecular "switch" that turns amyloid pathology into tau pathology, which could open the door to safer, cheaper disease-modifying therapies.
Alzheimer's research zeroes in on the amyloid-to-tau transition — and a new path to earlier treatment
At the 2026 Alzheimer's Association International Conference (AAIC) in London, Takaomi Saido, PhD, of RIKEN BIO in Japan, shared decades of research connecting neprilysin — the brain's primary amyloid-beta (Aβ) degrading enzyme — to the development of donanemab and the broader quest to stop Alzheimer's disease (AD) before it starts. His work suggests that somatostatin, a brain signaling molecule, regulates neprilysin expression, potentially offering a new lever to control Aβ accumulation during the preclinical stage of AD.
Saido's team is now focused on identifying the molecular mechanisms responsible for the transition from Aβ pathology to tau pathology — the step widely believed to drive neurodegeneration and cognitive decline. Using next-generation mouse models designed to better reflect human AD biology, researchers observed distinct tau progression patterns depending on the tau mutation studied, suggesting multiple pathways may be at play.
Key Takeaways
Why it matters: Current Alzheimer's therapies intervene late in the disease course. Identifying the molecular triggers that link amyloid to tau pathology could enable truly preventive treatments — a potential game-changer for millions at risk.
