Scientists at Sanford Burnham Prebys reported in Science Advances that SORLA upregulation suppressed multiple pathological features in an aged tauopathy mouse model. The study centers on tau tangles and synaptic loss—hallmarks of tau-driven neurodegeneration—and positions SORLA as a potential therapeutic target. In the paper, investigators led by Timothy Huang, PhD, describe experiments showing that increasing SORLA activity protected against the downstream effects of pathological tau biology in vivo. The authors frame the work as building on prior evidence that SORLA can reduce amyloid-beta generation, while clarifying whether SORLA also modulates tau pathology. SORLA is described as a trafficking receptor expressed in neurons and glia in both mouse and human brain. Huang said the findings reveal a protective role for SORLA across multiple aspects of tauopathy pathogenesis. The work remains preclinical, but it adds a target with in vivo support in tauopathy models and highlights a pathway that could inform future therapeutic development.