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Cognitive neurology
Original research
Tau-PET imaging predicts cognitive decline and brain atrophy progression in early Alzheimer’s disease
  1. Julien Lagarde1,2,3,
  2. Pauline Olivieri1,2,3,
  3. Matteo Tonietto3,
  4. Cecile Tissot4,
  5. Isabelle Rivals5,
  6. Philippe Gervais3,
  7. Fabien Caillé3,
  8. Martin Moussion1,6,
  9. Michel Bottlaender3,7,
  10. Marie Sarazin1,2,3
  1. 1 Department of Neurology of Memory and Language, GHU Paris Psychiatrie & Neurosciences, Hôpital Sainte-Anne, Paris, France
  2. 2 Université de Paris, Paris, France
  3. 3 Université Paris-Saclay, BioMaps, Service Hospitalier Frédéric Joliot CEA, CNRS, Inserm, Orsay, France
  4. 4 McGill University Research Centre for Studies in Aging, Montreal, Quebec, Canada
  5. 5 Equipe de Statistique Appliquée, ESPCI Paris, PSL Research University, INSERM, UMRS 1158 Neurophysiologie Respiratoire Expérimentale et Clinique, 10 rue Vauquelin, Paris, France
  6. 6 Centre d'évaluation Troubles Psychiques et Vieillissement, GHU Paris Psychiatrie & Neurosciences, Hôpital Sainte-Anne, Paris, France
  7. 7 Université Paris-Saclay, UNIACT, Neurospin, Joliot Institute, CEA, Gif sur Yvette, France
  1. Correspondence to Dr Julien Lagarde, Department of Neurology of Memory and Language, GHU Paris Psychiatrie & Neurosciences, Hôpital Sainte-Anne, Paris, France; j.lagarde{at}ghu-paris.fr

Abstract

Objectives To explore whether regional tau binding measured at baseline is associated with the rapidity of Alzheimer’s disease (AD) progression over 2 years, as assessed by the decline in specified cognitive domains, and the progression of regional brain atrophy, in comparison with amyloid-positron emission tomography (PET), MRI and cerebrospinal fluid (CSF) biomarkers.

Methods Thirty-six patients with AD (positive CSF biomarkers and amyloid-PET) and 15 controls underwent a complete neuropsychological assessment, 3T brain MRI, [11C]-PiB and [18F]-flortaucipir PET imaging, and were monitored annually over 2 years, with a second brain MRI after 2 years. We used mixed effects models to explore the relations between tau-PET, amyloid-PET, CSF biomarkers and MRI at baseline and cognitive decline and the progression of brain atrophy over 2 years in patients with AD.

Results Baseline tau-PET was strongly associated with the subsequent cognitive decline in regions that are usually associated with each cognitive domain. No significant relationship was observed between the cognitive decline and initial amyloid load, regional cortical atrophy or CSF biomarkers. Baseline tau tracer binding in the superior temporal gyrus was associated with subsequent atrophy in an inferomedial temporal volume of interest, as was the voxelwise tau tracer binding with subsequent cortical atrophy in the superior temporal, parietal and frontal association cortices.

Conclusions These results suggest that tau tracer binding is predictive of cognitive decline in AD in domain-specific brain areas, which provides important insights into the interaction between tau burden and neurodegeneration, and is of the utmost importance to develop new prognostic markers that will help improve the design of therapeutic trials.

  • PET
  • Alzheimer's disease
  • MRI

Data availability statement

Data are available on reasonable request.

https://doi.org/10.1136/jnnp-2021-328623

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    Data availability statement

    Data are available on reasonable request.

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    Footnotes

    • Contributors JL, MS and MB designed the work; acquired, analysed and interpreted the data and drafted the manuscript. PO analysed and interpreted the data, revised the manuscript and approved its final version. MT analysed and interpreted the data, revised the manuscript and approved its final version. CT and IR were involved in data analysis, revised the manuscript and approved its final version. PG, FC and MM were involved in data acquisition, revised the manuscript and approved its final version. Authors responsible for the overall content as the guarantors: JL and MS

    • Funding This study was funded by French Ministry of Health grant (PHRC-2013-0919), CEA (no award/grant number), Fondation pour la recherche sur la maladie d’Alzheimer (no award/grant number), Institut de Recherches Internationales Servier (no award/grant number), France-Alzheimer (no award/grant number).

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.