TY - JOUR
T1 - Remote network for cognitive symptoms derived from tau accumulation in progressive supranuclear palsy
AU - Hori, Yuki
AU - Endo, Hironobu
AU - Tagai, Kenji
AU - Kataoka, Yuko
AU - Goto, Ryoji
AU - Kurose, Shin
AU - Momota, Yuki
AU - Kokubo, Naomi
AU - Seki, Chie
AU - Moriguchi, Sho
AU - Shimada, Hitoshi
AU - Shinotoh, Hitoshi
AU - Tokuda, Takahiko
AU - Takahata, Keisuke
AU - Minamimoto, Takafumi
AU - Higuchi, Makoto
AU - Hirabayashi, Toshiyuki
N1 - Publisher Copyright:
© 2026 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).
PY - 2026/7/10
Y1 - 2026/7/10
N2 - Progressive supranuclear palsy (PSP) is a neurodegenerative disorder with motor and cognitive impairments. Whereas motor symptoms are associated with subcortical tau deposits, the mechanisms underlying the cognitive symptoms remain unclear due to heterogeneous and primarily subcortical distribution of pathological tau deposits. Here, we combined tau-PET (tau positron emission tomography) using a high-contrast probe we developed with a normative connectome in 37 patients with PSP and 48 healthy controls. We found that tau deposition sites functionally connected to a common cortical network that could not be derived from atrophy. This network predominantly overlapped with canonical action-mode and frontoparietal networks, which support adaptive, goal-directed behavior. Whereas the extent of primary tau deposition predicted motor symptoms, the normative connectivity strength from tau deposition sites to the identified cortical network explained the severity of cognitive deficits. These findings suggest a previously unknown mechanism that cognitive, but not motor, deficits in PSP arise from remote effects of tau deposition—independent of atrophy—via convergent connectivity to a common cortical network.
AB - Progressive supranuclear palsy (PSP) is a neurodegenerative disorder with motor and cognitive impairments. Whereas motor symptoms are associated with subcortical tau deposits, the mechanisms underlying the cognitive symptoms remain unclear due to heterogeneous and primarily subcortical distribution of pathological tau deposits. Here, we combined tau-PET (tau positron emission tomography) using a high-contrast probe we developed with a normative connectome in 37 patients with PSP and 48 healthy controls. We found that tau deposition sites functionally connected to a common cortical network that could not be derived from atrophy. This network predominantly overlapped with canonical action-mode and frontoparietal networks, which support adaptive, goal-directed behavior. Whereas the extent of primary tau deposition predicted motor symptoms, the normative connectivity strength from tau deposition sites to the identified cortical network explained the severity of cognitive deficits. These findings suggest a previously unknown mechanism that cognitive, but not motor, deficits in PSP arise from remote effects of tau deposition—independent of atrophy—via convergent connectivity to a common cortical network.
UR - https://www.scopus.com/pages/publications/105044987782
UR - https://www.scopus.com/pages/publications/105044987782#tab=citedBy
U2 - 10.1126/sciadv.aed0348
DO - 10.1126/sciadv.aed0348
M3 - Article
C2 - 42430462
AN - SCOPUS:105044987782
SN - 2375-2548
VL - 12
SP - 1
EP - 12
JO - Science advances
JF - Science advances
IS - 28
M1 - eaed0348
ER -