Functional brain architecture is associated with the rate of tau accumulation in Alzheimer’s disease

doi:10.1038/s41467-019-14159-1

Functional brain architecture is associated with the rate of tau accumulation in Alzheimer’s disease

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282 Citas (Scopus)

Resumen

In Alzheimer’s diseases (AD), tau pathology is strongly associated with cognitive decline. Preclinical evidence suggests that tau spreads across connected neurons in an activity-dependent manner. Supporting this, cross-sectional AD studies show that tau deposition patterns resemble functional brain networks. However, whether higher functional connectivity is associated with higher rates of tau accumulation is unclear. Here, we combine resting-state fMRI with longitudinal tau-PET in two independent samples including 53 (ADNI) and 41 (BioFINDER) amyloid-biomarker defined AD subjects and 28 (ADNI) vs. 16 (BioFINDER) amyloid-negative healthy controls. In both samples, AD subjects show faster tau accumulation than controls. Second, in AD, higher fMRI-assessed connectivity between 400 regions of interest (ROIs) is associated with correlated tau-PET accumulation in corresponding ROIs. Third, we show that a model including baseline connectivity and tau-PET is associated with future tau-PET accumulation. Together, connectivity is associated with tau spread in AD, supporting the view of transneuronal tau propagation.

Idioma original	English
Número de artículo	347
Publicación	Nature Communications
Volumen	11
N.º	1
DOI	https://doi.org/10.1038/s41467-019-14159-1
Estado	Published - dic 1 2020

Nota bibliográfica

Publisher Copyright:
© 2020, The Author(s).

Financiación

Parts of the data used in preparation of this manuscript were obtained from the ADNI database (adni. loni.usc.edu). As such, the investigators within the ADNI study contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this paper. A complete listing of ADNI investigators can be found at the end of the manuscript. The study was funded by grants from the Alzheimer Forschung Initiative (AFI, Grant 15035 to M.E.), European Commission (Grant 334259 to M.E.), LMU excellence (AOST 865297 to M.E.) and Förderung Forschung Lehre (1032 to N.F.). ADNI data collection and sharing for this project was funded by the ADNI (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging, and Bioengineering, and through contributions from the following: AbbVie, Alzheimer’s Association; Alzheimer’s Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosity; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (www.fnih.org).

Financiadores	Número del financiador
National Institute of Biomedical Imaging and Bioengineering
National Institutes of Health (NIH)
European Commission
DoD Alzheimer's Disease Neuroimaging Initiative
DOD ADNI
U.S. Department of Health & Human Services \| NIH \| National Institute on Aging (U.S. National Institute on Aging)	P30AG062715, U19AG024904
LMU excellence	1032, AOST 865297
Alzheimer Forschung Initiative	15035
Seventh Framework Programme	334259
National Center for Advancing Translational Sciences (NCATS)	UL1TR002369
U.S. Department of Defense	W81XWH-12-2-0012

ASJC Scopus subject areas

General Chemistry
General Biochemistry, Genetics and Molecular Biology
General
General Physics and Astronomy

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10.1038/s41467-019-14159-1

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@article{2549de7956794413bfaa43096fedfb35,

title = "Functional brain architecture is associated with the rate of tau accumulation in Alzheimer{\textquoteright}s disease",

abstract = "In Alzheimer{\textquoteright}s diseases (AD), tau pathology is strongly associated with cognitive decline. Preclinical evidence suggests that tau spreads across connected neurons in an activity-dependent manner. Supporting this, cross-sectional AD studies show that tau deposition patterns resemble functional brain networks. However, whether higher functional connectivity is associated with higher rates of tau accumulation is unclear. Here, we combine resting-state fMRI with longitudinal tau-PET in two independent samples including 53 (ADNI) and 41 (BioFINDER) amyloid-biomarker defined AD subjects and 28 (ADNI) vs. 16 (BioFINDER) amyloid-negative healthy controls. In both samples, AD subjects show faster tau accumulation than controls. Second, in AD, higher fMRI-assessed connectivity between 400 regions of interest (ROIs) is associated with correlated tau-PET accumulation in corresponding ROIs. Third, we show that a model including baseline connectivity and tau-PET is associated with future tau-PET accumulation. Together, connectivity is associated with tau spread in AD, supporting the view of transneuronal tau propagation.",

author = "Nicolai Franzmeier and Julia Neitzel and Anna Rubinski and Ruben Smith and Olof Strandberg and Rik Ossenkoppele and Oskar Hansson and Michael Ewers and Michael Weiner and Paul Aisen and Ronald Petersen and Jack, \{Clifford R.\} and William Jagust and Trojanowki, \{John Q.\} and Toga, \{Arthur W.\} and Laurel Beckett and Green, \{Robert C.\} and Saykin, \{Andrew J.\} and Morris, \{John C.\} and Shaw, \{Leslie M.\} and Enchi Liu and Tom Montine and Thomas, \{Ronald G.\} and Michael Donohue and Sarah Walter and Devon Gessert and Tamie Sather and Gus Jiminez and Danielle Harvey and Michael Donohue and Matthew Bernstein and Nick Fox and Paul Thompson and Norbert Schuff and Charles DeCArli and Bret Borowski and Jeff Gunter and Matt Senjem and Prashanthi Vemuri and David Jones and Kejal Kantarci and Chad Ward and Koeppe, \{Robert A.\} and Norm Foster and Reiman, \{Eric M.\} and Kewei Chen and Chet Mathis and Susan Landau and Greg Jicha and Richard King",

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AU - Neitzel, Julia

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AU - Ossenkoppele, Rik

AU - Hansson, Oskar

AU - Ewers, Michael

AU - Weiner, Michael

AU - Aisen, Paul

AU - Petersen, Ronald

AU - Jack, Clifford R.

AU - Jagust, William

AU - Trojanowki, John Q.

AU - Toga, Arthur W.

AU - Beckett, Laurel

AU - Green, Robert C.

AU - Saykin, Andrew J.

AU - Morris, John C.

AU - Shaw, Leslie M.

AU - Liu, Enchi

AU - Montine, Tom

AU - Thomas, Ronald G.

AU - Donohue, Michael

AU - Walter, Sarah

AU - Gessert, Devon

AU - Sather, Tamie

AU - Jiminez, Gus

AU - Harvey, Danielle

AU - Donohue, Michael

AU - Bernstein, Matthew

AU - Fox, Nick

AU - Thompson, Paul

AU - Schuff, Norbert

AU - DeCArli, Charles

AU - Borowski, Bret

AU - Gunter, Jeff

AU - Senjem, Matt

AU - Vemuri, Prashanthi

AU - Jones, David

AU - Kantarci, Kejal

AU - Ward, Chad

AU - Koeppe, Robert A.

AU - Foster, Norm

AU - Reiman, Eric M.

AU - Chen, Kewei

AU - Mathis, Chet

AU - Landau, Susan

AU - Jicha, Greg

AU - King, Richard

PY - 2020/12/1

Y1 - 2020/12/1

N2 - In Alzheimer’s diseases (AD), tau pathology is strongly associated with cognitive decline. Preclinical evidence suggests that tau spreads across connected neurons in an activity-dependent manner. Supporting this, cross-sectional AD studies show that tau deposition patterns resemble functional brain networks. However, whether higher functional connectivity is associated with higher rates of tau accumulation is unclear. Here, we combine resting-state fMRI with longitudinal tau-PET in two independent samples including 53 (ADNI) and 41 (BioFINDER) amyloid-biomarker defined AD subjects and 28 (ADNI) vs. 16 (BioFINDER) amyloid-negative healthy controls. In both samples, AD subjects show faster tau accumulation than controls. Second, in AD, higher fMRI-assessed connectivity between 400 regions of interest (ROIs) is associated with correlated tau-PET accumulation in corresponding ROIs. Third, we show that a model including baseline connectivity and tau-PET is associated with future tau-PET accumulation. Together, connectivity is associated with tau spread in AD, supporting the view of transneuronal tau propagation.

AB - In Alzheimer’s diseases (AD), tau pathology is strongly associated with cognitive decline. Preclinical evidence suggests that tau spreads across connected neurons in an activity-dependent manner. Supporting this, cross-sectional AD studies show that tau deposition patterns resemble functional brain networks. However, whether higher functional connectivity is associated with higher rates of tau accumulation is unclear. Here, we combine resting-state fMRI with longitudinal tau-PET in two independent samples including 53 (ADNI) and 41 (BioFINDER) amyloid-biomarker defined AD subjects and 28 (ADNI) vs. 16 (BioFINDER) amyloid-negative healthy controls. In both samples, AD subjects show faster tau accumulation than controls. Second, in AD, higher fMRI-assessed connectivity between 400 regions of interest (ROIs) is associated with correlated tau-PET accumulation in corresponding ROIs. Third, we show that a model including baseline connectivity and tau-PET is associated with future tau-PET accumulation. Together, connectivity is associated with tau spread in AD, supporting the view of transneuronal tau propagation.

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DO - 10.1038/s41467-019-14159-1

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C2 - 31953405

AN - SCOPUS:85078065413

SN - 2041-1723

VL - 11

JO - Nature Communications

JF - Nature Communications

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ER -

Functional brain architecture is associated with the rate of tau accumulation in Alzheimer’s disease

Resumen

Nota bibliográfica

Financiación

ASJC Scopus subject areas

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