Researchers at the Buck Institute have uncovered that neuronal glycogen accumulation exacerbates tauopathies like Alzheimer’s disease by impairing oxidative stress management. Restoration of glycogen breakdown through enzymatic activation mitigated tau-related damage in fly and human models. The findings suggest new therapeutic avenues and provide insight into why GLP-1 receptor agonists might confer neuroprotection, linking sugar metabolism with neurodegenerative disease pathways.