Polygenic Effect on Tau Pathology Progression in Alzheimer's Disease.


Journal

Annals of neurology
ISSN: 1531-8249
Titre abrégé: Ann Neurol
Pays: United States
ID NLM: 7707449

Informations de publication

Date de publication:
04 2023
Historique:
revised: 02 11 2022
received: 23 06 2022
accepted: 19 12 2022
medline: 29 3 2023
pubmed: 27 12 2022
entrez: 26 12 2022
Statut: ppublish

Résumé

Polygenic variation accounts for a substantial portion of the risk of Alzheimer's disease (AD), but its effect on the rate of fibrillar-tau accumulation as a key driver of dementia symptoms is unclear. We combined the to-date largest number of genetic risk variants of AD (n = 85 lead single-nucleotide polymorphisms [SNPs]) from recent genome-wide association studies (GWAS) to generate a polygenic score (PGS). We assessed longitudinal tau-positron emission tomography (PET), amyloid-PET, and cognition in 231 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Using the PGS, together with global amyloid-PET, we predicted the rate of tau-PET increases in Braak-stage regions-of-interest and cognitive decline. We also assessed PGS-risk enrichment effects on the required sample size in clinical trials targeting tau pathology. We found that a higher PGS was associated with higher rates of tau-PET accumulation, in particular at elevated amyloid-PET levels. The tau-PET increases mediated the association between PGS and faster cognitive decline. Risk enrichment through high PGS afforded sample size savings by 34%. Our results demonstrate that the PGS predicts faster tau progression and thus cognitive decline, showing utility to enhance statistical power in clinical trials. ANN NEUROL 2023;93:819-829.

Identifiants

pubmed: 36571564
doi: 10.1002/ana.26588
doi:

Substances chimiques

tau Proteins 0
Biomarkers 0
Amyloid 0
Amyloid beta-Peptides 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

819-829

Subventions

Organisme : NIA NIH HHS
ID : U01 AG024904
Pays : United States

Informations de copyright

© 2022 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

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Auteurs

Anna Rubinski (A)

Institute for Stroke and Dementia Research, University Hospital, Ludwig Maximilian University, Munich, Germany.

Simon Frerich (S)

Institute for Stroke and Dementia Research, University Hospital, Ludwig Maximilian University, Munich, Germany.
Graduate School of Systemic Neurosciences, Ludwig Maximilian University, Munich, Germany.

Rainer Malik (R)

Institute for Stroke and Dementia Research, University Hospital, Ludwig Maximilian University, Munich, Germany.

Nicolai Franzmeier (N)

Institute for Stroke and Dementia Research, University Hospital, Ludwig Maximilian University, Munich, Germany.

Alfredo Ramirez (A)

Division of Neurogenetics and Molecular Psychiatry, Department of Psychiatry and Psychotherapy, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Department of Neurodegenerative diseases and Geriatric Psychiatry, University Hospital Bonn, Medical Faculty, Bonn, Germany.
Department of Psychiatry and Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX.
German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Cluster of Excellence Cellular Stress Responses in Aging-associated Diseases (CECAD), University of Cologne, Cologne, Germany.

Martin Dichgans (M)

Institute for Stroke and Dementia Research, University Hospital, Ludwig Maximilian University, Munich, Germany.
German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.

Michael Ewers (M)

Institute for Stroke and Dementia Research, University Hospital, Ludwig Maximilian University, Munich, Germany.
German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.

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