Tau deposition patterns are associated with functional connectivity in primary tauopathies

Nicolai Franzmeier; Matthias Brendel; Leonie Beyer; Luna Slemann; Gabor G. Kovacs; Thomas Arzberger; Carolin Kurz; Gesine Respondek; Milica J. Lukic; Davina Biel; Anna Rubinski; Lukas Frontzkowski; Selina Hummel; Andre Müller; Anika Finze; Carla Palleis; Emanuel Joseph; Endy Weidinger; Sabrina Katzdobler; Mengmeng Song; Gloria Biechele; Maike Kern; Maximilian Scheifele; Boris Stephan Rauchmann; Robert Perneczky; Michael Rullman; Marianne Patt; Andreas Schildan; Henryk Barthel; Osama Sabri; Jost J. Rumpf; Matthias L. Schroeter; Joseph Classen; Victor Villemagne; John Seibyl; Andrew W. Stephens; Edward B. Lee; David G. Coughlin; Armin Giese; Murray Grossman; Corey T. McMillan; Ellen Gelpi; Laura Molina-Porcel; Yaroslau Compta; John C. van Swieten; Laura Donker Laat; Claire Troakes; Safa Al-Sarraj; John L. Robinson; Sharon X. Xie; David J. Irwin; Sigrun Roeber; Jochen Herms; Mikael Simons; Peter Bartenstein; Virginia M. Lee; John Q. Trojanowski; Johannes Levin; Günter Höglinger; Michael Ewers

doi:10.1038/s41467-022-28896-3

Tau deposition patterns are associated with functional connectivity in primary tauopathies

Nicolai Franzmeier^*
, Matthias Brendel
, Leonie Beyer
, Luna Slemann
, Gabor G. Kovacs
, Thomas Arzberger
, Carolin Kurz
, Gesine Respondek
, Milica J. Lukic
, Davina Biel
, Anna Rubinski
, Lukas Frontzkowski
, Selina Hummel
, Andre Müller
, Anika Finze
, Carla Palleis
, Emanuel Joseph
, Endy Weidinger
, Sabrina Katzdobler
, Mengmeng Song

Gloria Biechele, Maike Kern, Maximilian Scheifele, Boris Stephan Rauchmann, Robert Perneczky, Michael Rullman, Marianne Patt, Andreas Schildan, Henryk Barthel, Osama Sabri, Jost J. Rumpf, Matthias L. Schroeter, Joseph Classen, Victor Villemagne, John Seibyl, Andrew W. Stephens, Edward B. Lee, David G. Coughlin, Armin Giese, Murray Grossman, Corey T. McMillan, Ellen Gelpi, Laura Molina-Porcel, Yaroslau Compta, John C. van Swieten, Laura Donker Laat, Claire Troakes, Safa Al-Sarraj, John L. Robinson, Sharon X. Xie, David J. Irwin, Sigrun Roeber, Jochen Herms, Mikael Simons, Peter Bartenstein, Virginia M. Lee, John Q. Trojanowski, Johannes Levin, Günter Höglinger, Michael Ewers

^*Corresponding author for this work

Neurology

Klinikum der Universität München
Munich Cluster for Systems Neurology (SyNergy)
University of Pennsylvania
University of Toronto
University Health Network
German Center for Neurodegenerative Diseases
Ludwig Maximilian University of Munich
Klinikum rechts der Isar der Technischen Universität München
Hannover Medical School
University of Belgrade
Life Molecular Imaging GmbH
Imperial College London
University Hospital Leipzig
University Hospital Cologne
University of Melbourne
University of Pittsburgh School of Medicine
InviCRO, LLC
inviCRO
University of California at San Diego
University of Barcelona
Medical University of Vienna
Erasmus University Rotterdam
King's College London

Research output: Contribution to journal › Article › Academic › peer-review

102 Citations (Scopus)

72 Downloads (Pure)

Abstract

Tau pathology is the main driver of neuronal dysfunction in 4-repeat tauopathies, including cortico-basal degeneration and progressive supranuclear palsy. Tau is assumed to spread prion-like across connected neurons, but the mechanisms of tau propagation are largely elusive in 4-repeat tauopathies, characterized not only by neuronal but also by astroglial and oligodendroglial tau accumulation. Here, we assess whether connectivity is associated with 4R-tau deposition patterns by combining resting-state fMRI connectomics with both 2^nd generation ¹⁸F-PI-2620 tau-PET in 46 patients with clinically diagnosed 4-repeat tauopathies and post-mortem cell-type-specific regional tau assessments from two independent progressive supranuclear palsy patient samples (n = 97 and n = 96). We find that inter-regional connectivity is associated with higher inter-regional correlation of both tau-PET and post-mortem tau levels in 4-repeat tauopathies. In regional cell-type specific post-mortem tau assessments, this association is stronger for neuronal than for astroglial or oligodendroglial tau, suggesting that connectivity is primarily associated with neuronal tau accumulation. Using tau-PET we find further that patient-level tau patterns are associated with the connectivity of subcortical tau epicenters. Together, the current study provides combined in vivo tau-PET and histopathological evidence that brain connectivity is associated with tau deposition patterns in 4-repeat tauopathies.

Original language	English
Article number	1362
Journal	Nature Communications
Volume	13
Issue number	1
DOIs	https://doi.org/10.1038/s41467-022-28896-3
Publication status	Published - 15 Mar 2022

Bibliographical note

Funding Information:
We acknowledge all members of the German Imaging Initiative for Tauopathies (GII4T) and the Alzheimer’s Disease Neuroimaging Initiative (see supplementary information for a list of consortium members). We wish to thank the patients and their families, without whose support and altruism this research would not have been possible. Further, we would like to acknowledge Prof. Christian Haass (DZNE, Munich) for his consultation on study design, the European Reference Network for Rare Neurological Diseases—Project ID No 739510 and the Neurological Tissue Bank of the Biobanc-Hospital Clinic-IDIBAPS for sample and data procurement. This work was supported by the NIH (P30AG010124, P01AG066597, U19AG062418, and R01-NS109260), the National Center for Advancing Translational Sciences (TL1TR001880), the German Research Foundation (DFG; SCHR 774/5-1, DFG, INST 409/193-1 FUGG) the SyNergy excellence cluster (EXC 2145/ID 390857198). N.F. was supported by the Hertie foundation for clinical neurosciences. G.G.K. is supported by the Rossy Foundation and Safra Foundation. G.H. was funded by the Deutsche Forschungsgemeinschaft (DFG, HO2402/18-1 MSAomics), the German Federal Ministry of Education and Research (BMBF, 01EK1605A HitTau), VolkswagenStiftung and Lower Saxony Ministry for Science (Niedersächsisches Vorab), Petermax-Müller Foundation (Etiology and Therapy of Synucleinopathies and Tauopathies). M.B. was supported by the Hirnliga e.V. (Manfred-Strohscheer-Stiftung) and by the Alzheimer Forschung Initiative e.V. (grant number #19063p).

Funding Information:
We acknowledge all members of the German Imaging Initiative for Tauopathies (GII4T) and the Alzheimer’s Disease Neuroimaging Initiative (see supplementary information for a list of consortium members). We wish to thank the patients and their families, without whose support and altruism this research would not have been possible. Further, we would like to acknowledge Prof. Christian Haass (DZNE, Munich) for his consultation on study design, the European Reference Network for Rare Neurological Diseases—Project ID No 739510 and the Neurological Tissue Bank of the Biobanc-Hospital Clinic-IDIBAPS for sample and data procurement. This work was supported by the NIH (P30AG010124, P01AG066597, U19AG062418, and R01-NS109260), the National Center for Advancing Translational Sciences (TL1TR001880), the German Research Foundation (DFG; SCHR 774/5-1, DFG, INST 409/193-1 FUGG) the SyNergy excellence cluster (EXC 2145/ID 390857198). N.F. was supported by the Hertie foundation for clinical neurosciences. G.G.K. is supported by the Rossy Foundation and Safra Foundation. G.H. was funded by the Deutsche Forschungsgemeinschaft (DFG, HO2402/18-1 MSAomics), the German Federal Ministry of Education and Research (BMBF, 01EK1605A HitTau), VolkswagenStiftung and Lower Saxony Ministry for Science (Niedersächsisches Vorab), Petermax-Müller Foundation (Etiology and Therapy of Synucleinopathies and Tauopathies). M.B. was supported by the Hirnliga e.V. (Manfred-Strohscheer-Stiftung) and by the Alzheimer Forschung Initiative e.V. (grant number #19063p).

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© 2022, The Author(s).

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Tau deposition patterns are associated with functional connectivity in primary tauopathiesFinal published version, 7.5 MBLicence: CC BY

Cite this

Franzmeier, N., Brendel, M., Beyer, L., Slemann, L., Kovacs, G. G., Arzberger, T., Kurz, C., Respondek, G., Lukic, M. J., Biel, D., Rubinski, A., Frontzkowski, L., Hummel, S., Müller, A., Finze, A., Palleis, C., Joseph, E., Weidinger, E., Katzdobler, S., ... Ewers, M. (2022). Tau deposition patterns are associated with functional connectivity in primary tauopathies. Nature Communications, 13(1), Article 1362. https://doi.org/10.1038/s41467-022-28896-3

@article{ad3f72edb23d463385d2e6da341194bb,

title = "Tau deposition patterns are associated with functional connectivity in primary tauopathies",

abstract = "Tau pathology is the main driver of neuronal dysfunction in 4-repeat tauopathies, including cortico-basal degeneration and progressive supranuclear palsy. Tau is assumed to spread prion-like across connected neurons, but the mechanisms of tau propagation are largely elusive in 4-repeat tauopathies, characterized not only by neuronal but also by astroglial and oligodendroglial tau accumulation. Here, we assess whether connectivity is associated with 4R-tau deposition patterns by combining resting-state fMRI connectomics with both 2nd generation 18F-PI-2620 tau-PET in 46 patients with clinically diagnosed 4-repeat tauopathies and post-mortem cell-type-specific regional tau assessments from two independent progressive supranuclear palsy patient samples (n = 97 and n = 96). We find that inter-regional connectivity is associated with higher inter-regional correlation of both tau-PET and post-mortem tau levels in 4-repeat tauopathies. In regional cell-type specific post-mortem tau assessments, this association is stronger for neuronal than for astroglial or oligodendroglial tau, suggesting that connectivity is primarily associated with neuronal tau accumulation. Using tau-PET we find further that patient-level tau patterns are associated with the connectivity of subcortical tau epicenters. Together, the current study provides combined in vivo tau-PET and histopathological evidence that brain connectivity is associated with tau deposition patterns in 4-repeat tauopathies.",

author = "Nicolai Franzmeier and Matthias Brendel and Leonie Beyer and Luna Slemann and Kovacs, \{Gabor G.\} and Thomas Arzberger and Carolin Kurz and Gesine Respondek and Lukic, \{Milica J.\} and Davina Biel and Anna Rubinski and Lukas Frontzkowski and Selina Hummel and Andre M{\"u}ller and Anika Finze and Carla Palleis and Emanuel Joseph and Endy Weidinger and Sabrina Katzdobler and Mengmeng Song and Gloria Biechele and Maike Kern and Maximilian Scheifele and Rauchmann, \{Boris Stephan\} and Robert Perneczky and Michael Rullman and Marianne Patt and Andreas Schildan and Henryk Barthel and Osama Sabri and Rumpf, \{Jost J.\} and Schroeter, \{Matthias L.\} and Joseph Classen and Victor Villemagne and John Seibyl and Stephens, \{Andrew W.\} and Lee, \{Edward B.\} and Coughlin, \{David G.\} and Armin Giese and Murray Grossman and McMillan, \{Corey T.\} and Ellen Gelpi and Laura Molina-Porcel and Yaroslau Compta and \{van Swieten\}, \{John C.\} and Laat, \{Laura Donker\} and Claire Troakes and Safa Al-Sarraj and Robinson, \{John L.\} and Xie, \{Sharon X.\} and Irwin, \{David J.\} and Sigrun Roeber and Jochen Herms and Mikael Simons and Peter Bartenstein and Lee, \{Virginia M.\} and Trojanowski, \{John Q.\} and Johannes Levin and G{\"u}nter H{\"o}glinger and Michael Ewers",

note = "Funding Information: We acknowledge all members of the German Imaging Initiative for Tauopathies (GII4T) and the Alzheimer{\textquoteright}s Disease Neuroimaging Initiative (see supplementary information for a list of consortium members). We wish to thank the patients and their families, without whose support and altruism this research would not have been possible. Further, we would like to acknowledge Prof. Christian Haass (DZNE, Munich) for his consultation on study design, the European Reference Network for Rare Neurological Diseases{\textemdash}Project ID No 739510 and the Neurological Tissue Bank of the Biobanc-Hospital Clinic-IDIBAPS for sample and data procurement. This work was supported by the NIH (P30AG010124, P01AG066597, U19AG062418, and R01-NS109260), the National Center for Advancing Translational Sciences (TL1TR001880), the German Research Foundation (DFG; SCHR 774/5-1, DFG, INST 409/193-1 FUGG) the SyNergy excellence cluster (EXC 2145/ID 390857198). N.F. was supported by the Hertie foundation for clinical neurosciences. G.G.K. is supported by the Rossy Foundation and Safra Foundation. G.H. was funded by the Deutsche Forschungsgemeinschaft (DFG, HO2402/18-1 MSAomics), the German Federal Ministry of Education and Research (BMBF, 01EK1605A HitTau), VolkswagenStiftung and Lower Saxony Ministry for Science (Nieders{\"a}chsisches Vorab), Petermax-M{\"u}ller Foundation (Etiology and Therapy of Synucleinopathies and Tauopathies). M.B. was supported by the Hirnliga e.V. (Manfred-Strohscheer-Stiftung) and by the Alzheimer Forschung Initiative e.V. (grant number \#19063p). Funding Information: We acknowledge all members of the German Imaging Initiative for Tauopathies (GII4T) and the Alzheimer{\textquoteright}s Disease Neuroimaging Initiative (see supplementary information for a list of consortium members). We wish to thank the patients and their families, without whose support and altruism this research would not have been possible. Further, we would like to acknowledge Prof. Christian Haass (DZNE, Munich) for his consultation on study design, the European Reference Network for Rare Neurological Diseases{\textemdash}Project ID No 739510 and the Neurological Tissue Bank of the Biobanc-Hospital Clinic-IDIBAPS for sample and data procurement. This work was supported by the NIH (P30AG010124, P01AG066597, U19AG062418, and R01-NS109260), the National Center for Advancing Translational Sciences (TL1TR001880), the German Research Foundation (DFG; SCHR 774/5-1, DFG, INST 409/193-1 FUGG) the SyNergy excellence cluster (EXC 2145/ID 390857198). N.F. was supported by the Hertie foundation for clinical neurosciences. G.G.K. is supported by the Rossy Foundation and Safra Foundation. G.H. was funded by the Deutsche Forschungsgemeinschaft (DFG, HO2402/18-1 MSAomics), the German Federal Ministry of Education and Research (BMBF, 01EK1605A HitTau), VolkswagenStiftung and Lower Saxony Ministry for Science (Nieders{\"a}chsisches Vorab), Petermax-M{\"u}ller Foundation (Etiology and Therapy of Synucleinopathies and Tauopathies). M.B. was supported by the Hirnliga e.V. (Manfred-Strohscheer-Stiftung) and by the Alzheimer Forschung Initiative e.V. (grant number \#19063p). Publisher Copyright: {\textcopyright} 2022, The Author(s).",

year = "2022",

month = mar,

day = "15",

doi = "10.1038/s41467-022-28896-3",

language = "English",

volume = "13",

journal = "Nature Communications",

issn = "2041-1723",

publisher = "Nature Research",

number = "1",

}

Franzmeier, N, Brendel, M, Beyer, L, Slemann, L, Kovacs, GG, Arzberger, T, Kurz, C, Respondek, G, Lukic, MJ, Biel, D, Rubinski, A, Frontzkowski, L, Hummel, S, Müller, A, Finze, A, Palleis, C, Joseph, E, Weidinger, E, Katzdobler, S, Song, M, Biechele, G, Kern, M, Scheifele, M, Rauchmann, BS, Perneczky, R, Rullman, M, Patt, M, Schildan, A, Barthel, H, Sabri, O, Rumpf, JJ, Schroeter, ML, Classen, J, Villemagne, V, Seibyl, J, Stephens, AW, Lee, EB, Coughlin, DG, Giese, A, Grossman, M, McMillan, CT, Gelpi, E, Molina-Porcel, L, Compta, Y, van Swieten, JC, Laat, LD, Troakes, C, Al-Sarraj, S, Robinson, JL, Xie, SX, Irwin, DJ, Roeber, S, Herms, J, Simons, M, Bartenstein, P, Lee, VM, Trojanowski, JQ, Levin, J, Höglinger, G & Ewers, M 2022, 'Tau deposition patterns are associated with functional connectivity in primary tauopathies', Nature Communications, vol. 13, no. 1, 1362. https://doi.org/10.1038/s41467-022-28896-3

TY - JOUR

T1 - Tau deposition patterns are associated with functional connectivity in primary tauopathies

AU - Franzmeier, Nicolai

AU - Brendel, Matthias

AU - Beyer, Leonie

AU - Slemann, Luna

AU - Kovacs, Gabor G.

AU - Arzberger, Thomas

AU - Kurz, Carolin

AU - Respondek, Gesine

AU - Lukic, Milica J.

AU - Biel, Davina

AU - Rubinski, Anna

AU - Frontzkowski, Lukas

AU - Hummel, Selina

AU - Müller, Andre

AU - Finze, Anika

AU - Palleis, Carla

AU - Joseph, Emanuel

AU - Weidinger, Endy

AU - Katzdobler, Sabrina

AU - Song, Mengmeng

AU - Biechele, Gloria

AU - Kern, Maike

AU - Scheifele, Maximilian

AU - Rauchmann, Boris Stephan

AU - Perneczky, Robert

AU - Rullman, Michael

AU - Patt, Marianne

AU - Schildan, Andreas

AU - Barthel, Henryk

AU - Sabri, Osama

AU - Rumpf, Jost J.

AU - Schroeter, Matthias L.

AU - Classen, Joseph

AU - Villemagne, Victor

AU - Seibyl, John

AU - Stephens, Andrew W.

AU - Lee, Edward B.

AU - Coughlin, David G.

AU - Giese, Armin

AU - Grossman, Murray

AU - McMillan, Corey T.

AU - Gelpi, Ellen

AU - Molina-Porcel, Laura

AU - Compta, Yaroslau

AU - van Swieten, John C.

AU - Laat, Laura Donker

AU - Troakes, Claire

AU - Al-Sarraj, Safa

AU - Robinson, John L.

AU - Xie, Sharon X.

AU - Irwin, David J.

AU - Roeber, Sigrun

AU - Herms, Jochen

AU - Simons, Mikael

AU - Bartenstein, Peter

AU - Lee, Virginia M.

AU - Trojanowski, John Q.

AU - Levin, Johannes

AU - Höglinger, Günter

AU - Ewers, Michael

N1 - Funding Information: We acknowledge all members of the German Imaging Initiative for Tauopathies (GII4T) and the Alzheimer’s Disease Neuroimaging Initiative (see supplementary information for a list of consortium members). We wish to thank the patients and their families, without whose support and altruism this research would not have been possible. Further, we would like to acknowledge Prof. Christian Haass (DZNE, Munich) for his consultation on study design, the European Reference Network for Rare Neurological Diseases—Project ID No 739510 and the Neurological Tissue Bank of the Biobanc-Hospital Clinic-IDIBAPS for sample and data procurement. This work was supported by the NIH (P30AG010124, P01AG066597, U19AG062418, and R01-NS109260), the National Center for Advancing Translational Sciences (TL1TR001880), the German Research Foundation (DFG; SCHR 774/5-1, DFG, INST 409/193-1 FUGG) the SyNergy excellence cluster (EXC 2145/ID 390857198). N.F. was supported by the Hertie foundation for clinical neurosciences. G.G.K. is supported by the Rossy Foundation and Safra Foundation. G.H. was funded by the Deutsche Forschungsgemeinschaft (DFG, HO2402/18-1 MSAomics), the German Federal Ministry of Education and Research (BMBF, 01EK1605A HitTau), VolkswagenStiftung and Lower Saxony Ministry for Science (Niedersächsisches Vorab), Petermax-Müller Foundation (Etiology and Therapy of Synucleinopathies and Tauopathies). M.B. was supported by the Hirnliga e.V. (Manfred-Strohscheer-Stiftung) and by the Alzheimer Forschung Initiative e.V. (grant number #19063p). Funding Information: We acknowledge all members of the German Imaging Initiative for Tauopathies (GII4T) and the Alzheimer’s Disease Neuroimaging Initiative (see supplementary information for a list of consortium members). We wish to thank the patients and their families, without whose support and altruism this research would not have been possible. Further, we would like to acknowledge Prof. Christian Haass (DZNE, Munich) for his consultation on study design, the European Reference Network for Rare Neurological Diseases—Project ID No 739510 and the Neurological Tissue Bank of the Biobanc-Hospital Clinic-IDIBAPS for sample and data procurement. This work was supported by the NIH (P30AG010124, P01AG066597, U19AG062418, and R01-NS109260), the National Center for Advancing Translational Sciences (TL1TR001880), the German Research Foundation (DFG; SCHR 774/5-1, DFG, INST 409/193-1 FUGG) the SyNergy excellence cluster (EXC 2145/ID 390857198). N.F. was supported by the Hertie foundation for clinical neurosciences. G.G.K. is supported by the Rossy Foundation and Safra Foundation. G.H. was funded by the Deutsche Forschungsgemeinschaft (DFG, HO2402/18-1 MSAomics), the German Federal Ministry of Education and Research (BMBF, 01EK1605A HitTau), VolkswagenStiftung and Lower Saxony Ministry for Science (Niedersächsisches Vorab), Petermax-Müller Foundation (Etiology and Therapy of Synucleinopathies and Tauopathies). M.B. was supported by the Hirnliga e.V. (Manfred-Strohscheer-Stiftung) and by the Alzheimer Forschung Initiative e.V. (grant number #19063p). Publisher Copyright: © 2022, The Author(s).

PY - 2022/3/15

Y1 - 2022/3/15

N2 - Tau pathology is the main driver of neuronal dysfunction in 4-repeat tauopathies, including cortico-basal degeneration and progressive supranuclear palsy. Tau is assumed to spread prion-like across connected neurons, but the mechanisms of tau propagation are largely elusive in 4-repeat tauopathies, characterized not only by neuronal but also by astroglial and oligodendroglial tau accumulation. Here, we assess whether connectivity is associated with 4R-tau deposition patterns by combining resting-state fMRI connectomics with both 2nd generation 18F-PI-2620 tau-PET in 46 patients with clinically diagnosed 4-repeat tauopathies and post-mortem cell-type-specific regional tau assessments from two independent progressive supranuclear palsy patient samples (n = 97 and n = 96). We find that inter-regional connectivity is associated with higher inter-regional correlation of both tau-PET and post-mortem tau levels in 4-repeat tauopathies. In regional cell-type specific post-mortem tau assessments, this association is stronger for neuronal than for astroglial or oligodendroglial tau, suggesting that connectivity is primarily associated with neuronal tau accumulation. Using tau-PET we find further that patient-level tau patterns are associated with the connectivity of subcortical tau epicenters. Together, the current study provides combined in vivo tau-PET and histopathological evidence that brain connectivity is associated with tau deposition patterns in 4-repeat tauopathies.

AB - Tau pathology is the main driver of neuronal dysfunction in 4-repeat tauopathies, including cortico-basal degeneration and progressive supranuclear palsy. Tau is assumed to spread prion-like across connected neurons, but the mechanisms of tau propagation are largely elusive in 4-repeat tauopathies, characterized not only by neuronal but also by astroglial and oligodendroglial tau accumulation. Here, we assess whether connectivity is associated with 4R-tau deposition patterns by combining resting-state fMRI connectomics with both 2nd generation 18F-PI-2620 tau-PET in 46 patients with clinically diagnosed 4-repeat tauopathies and post-mortem cell-type-specific regional tau assessments from two independent progressive supranuclear palsy patient samples (n = 97 and n = 96). We find that inter-regional connectivity is associated with higher inter-regional correlation of both tau-PET and post-mortem tau levels in 4-repeat tauopathies. In regional cell-type specific post-mortem tau assessments, this association is stronger for neuronal than for astroglial or oligodendroglial tau, suggesting that connectivity is primarily associated with neuronal tau accumulation. Using tau-PET we find further that patient-level tau patterns are associated with the connectivity of subcortical tau epicenters. Together, the current study provides combined in vivo tau-PET and histopathological evidence that brain connectivity is associated with tau deposition patterns in 4-repeat tauopathies.

UR - https://www.scopus.com/pages/publications/85126519547

U2 - 10.1038/s41467-022-28896-3

DO - 10.1038/s41467-022-28896-3

M3 - Article

C2 - 35292638

AN - SCOPUS:85126519547

SN - 2041-1723

VL - 13

JO - Nature Communications

JF - Nature Communications

IS - 1

M1 - 1362

ER -

Tau deposition patterns are associated with functional connectivity in primary tauopathies

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