Abstract 2
Category: Basic Science
At the end of the session, participants will be able to:
- Describe the details of nigral astrocytic tau pathology in PSP.
- Compare histopathological findings in the substantia nigra between NITAG and PSP cases.
- Explore possible differences between high- and low-groups of nigral tau-positive astrocytes in PSP.
COI Disclosure:
None to disclose.
Hidetomo Tanaka 1, Seojin Lee 1, Shelley L. Forrest 1, and Gabor G. Kovacs 1
1 Department of Laboratory Medicine and Pathobiology and Tanz Centre for Research in Neurodegenerative Disease, University of Toronto, Toronto, Ontario, Canada
Presenter
Hidetomo Tanaka, MD, PhD, is a Japanese neuropathologist. Through training of general internal medicine and neurology, he advanced toward neuropathology, completing specific training and research to obtain a PhD (neuropathology) from Niigata University (Japan). In 2022 he joined Dr. Kovacs lab at the University of Toronto. He holds the title of councilor in the Japanese Society of Neuropathology. His main interest is neurodegenerative diseases and conditions, with a focus on tauopathies.
Target Audience:
Pathologists, Residents
Medical Students
CanMEDS:
Scholar
Nigral astrocytic tau pathology in PSP
Abstract
Background: Astrocytic tau pathology is a major feature of primary tauopathies and aging-related tau astrogliopathy (ARTAG). Although tau pathology in the substantia nigra (SN) is usually neuronal, we recently reported cases with prominent nigral tau astrogliopathy (NITAG). Interestingly, despite diverse primary diseases, NITAG exhibited shared distinctive features: abundant tau-positive astrocytes with fewer tau-positive neuronal cytoplasmic inclusions (NCIs) and mild neuronal loss in the SN, and some astrocytic lesions in the other brainstem regions.
Method: We investigated the nigral astrocytic tau pathology in 39 progressive supranuclear palsy (PSP) cases.
Results: Compared to the cases with prominent NITAG, the severity of nigral astroglial tau pathology was not as high and was present in 36 of the 39 PSP cases, with varying amounts. We classified PSP cases into high and low groups based on the number of tau-positive astrocytes in the SN and compared clinicopathological features. Morphologically, nigral tau-positive astrocytes in PSP were distinct from typical tufted astrocytes and resembled those seen in NITAG. Unlike NITAG, both groups exhibited more than moderate neuronal loss and NCIs in the SN, with no significant difference. However, the extent of tau-positive astrocytes in midbrain regions outside the SN was significantly higher in the high-group.
Conclusion: We stratified PSP cases based on the presence and severity of NITAG-type pathology and identified distinct features supporting the notion that PSP might have different pathological subtypes eventually reflect distinct pathogenesis.