Researchers from the Buck Institute and collaborators have identified how neuronal glycogen breakdown mitigates tau pathology associated with neurodegenerative diseases like Alzheimer's and frontotemporal lobar degeneration. Their study, published in Nature Metabolism, reveals that glycogen accumulates in neurons with tauopathy, impairing oxidative stress management. Restoring glycogen phosphorylase activity reroutes sugar metabolism toward protective antioxidant pathways, reducing neuronal damage in fly and human models. These findings may explain the emerging protective effects of GLP-1 drugs against dementia, influencing future therapeutic strategies.