Alzheimer’s Disease and RNAi Therapeutics

Alzheimer’s disease (AD) affects over 50 million people globally, touching nearly every family. Traditionally, AD pathology has been defined by two hallmarks: extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles formed by hyperphosphorylated tau.

However, therapeutic strategies targeting amyloid alone have yielded only modest clinical benefits. Emerging research shows that AD involves a complex interplay between amyloid, tau, neuroinflammation, and T cell-mediated neurodegeneration.

Apolipoprotein E (ApoE)—the strongest genetic risk factor for AD—plays a central role in coordinating these pathways. We view ApoE as both a driver of disease and a high-value target for prevention and treatment.

Using divalent siRNA (di-siRNA), our lab has demonstrated significant reductions in amyloid and neuroinflammation in preclinical models. This AD research is one of our core programs, and we welcome passionate students and postdocs to join us in advancing it.

We have also developed a proprietary di-siRNA scaffold capable of simultaneously modulating multiple disease-relevant pathways. Given the interconnectivity of AD pathology, this multi-target approach holds promise for delivering truly disease-modifying treatments.