Since astroglial spinal cord AT8-tau pathology, as well as typical peripheral motor neuron symptomatology, were largely absent from both the upper and lower extremities in our cases, we can speculate that in PSP, glial dysfunction, rather than NTs or NCIs, in other areas of the pyramidal tract may be primarily responsible for PSP pathogenesis and clinical symptomatology. This evidence concerns the gene MAPT and supranuclear palsy, progressive, 1.