Combining tau-PET and fMRI meta-analyses for patient-centered prediction of cognitive decline in Alzheimer's disease.


Journal

Alzheimer's research & therapy
ISSN: 1758-9193
Titre abrégé: Alzheimers Res Ther
Pays: England
ID NLM: 101511643

Informations de publication

Date de publication:
07 11 2022
Historique:
received: 20 06 2022
accepted: 20 10 2022
entrez: 8 11 2022
pubmed: 9 11 2022
medline: 10 11 2022
Statut: epublish

Résumé

Tau-PET is a prognostic marker for cognitive decline in Alzheimer's disease, and the heterogeneity of tau-PET patterns matches cognitive symptom heterogeneity. Thus, tau-PET may allow precision-medicine prediction of individual tau-related cognitive trajectories, which can be important for determining patient-specific cognitive endpoints in clinical trials. Here, we aimed to examine whether tau-PET in cognitive-domain-specific brain regions, identified via fMRI meta-analyses, allows the prediction of domain-specific cognitive decline. Further, we aimed to determine whether tau-PET-informed personalized cognitive composites capture patient-specific cognitive trajectories more sensitively than conventional cognitive measures. We included Alzheimer's Disease Neuroimaging Initiative (ADNI) participants classified as controls (i.e., amyloid-negative, cognitively normal, n = 121) or Alzheimer's disease-spectrum (i.e., amyloid-positive, cognitively normal to dementia, n = 140), plus 111 AVID-1451-A05 participants for independent validation (controls/Alzheimer's disease-spectrum=46/65). All participants underwent baseline In both amyloid-positive cohorts (ADNI [age = 75.99±7.69] and A05 [age = 74.03±9.03]), cognitive-domain-specific tau-PET outperformed global and temporal-lobe tau-PET for predicting future cognitive decline in episodic memory, language, executive functioning, and visuospatial abilities. Further, a tau-PET-informed personalized cognitive composite across cognitive domains enhanced the sensitivity to assess cognitive decline in amyloid-positive subjects, yielding lower sample sizes required for detecting simulated intervention effects compared to conventional cognitive endpoints (i.e., memory composite, global cognitive composite). However, the latter effect was less strong in A05 compared to the ADNI cohort. Combining tau-PET with task-fMRI-derived maps of major cognitive domains facilitates the prediction of domain-specific cognitive decline. This approach may help to increase the sensitivity to detect Alzheimer's disease-related cognitive decline and to determine personalized cognitive endpoints in clinical trials.

Sections du résumé

BACKGROUND
Tau-PET is a prognostic marker for cognitive decline in Alzheimer's disease, and the heterogeneity of tau-PET patterns matches cognitive symptom heterogeneity. Thus, tau-PET may allow precision-medicine prediction of individual tau-related cognitive trajectories, which can be important for determining patient-specific cognitive endpoints in clinical trials. Here, we aimed to examine whether tau-PET in cognitive-domain-specific brain regions, identified via fMRI meta-analyses, allows the prediction of domain-specific cognitive decline. Further, we aimed to determine whether tau-PET-informed personalized cognitive composites capture patient-specific cognitive trajectories more sensitively than conventional cognitive measures.
METHODS
We included Alzheimer's Disease Neuroimaging Initiative (ADNI) participants classified as controls (i.e., amyloid-negative, cognitively normal, n = 121) or Alzheimer's disease-spectrum (i.e., amyloid-positive, cognitively normal to dementia, n = 140), plus 111 AVID-1451-A05 participants for independent validation (controls/Alzheimer's disease-spectrum=46/65). All participants underwent baseline
RESULTS
In both amyloid-positive cohorts (ADNI [age = 75.99±7.69] and A05 [age = 74.03±9.03]), cognitive-domain-specific tau-PET outperformed global and temporal-lobe tau-PET for predicting future cognitive decline in episodic memory, language, executive functioning, and visuospatial abilities. Further, a tau-PET-informed personalized cognitive composite across cognitive domains enhanced the sensitivity to assess cognitive decline in amyloid-positive subjects, yielding lower sample sizes required for detecting simulated intervention effects compared to conventional cognitive endpoints (i.e., memory composite, global cognitive composite). However, the latter effect was less strong in A05 compared to the ADNI cohort.
CONCLUSION
Combining tau-PET with task-fMRI-derived maps of major cognitive domains facilitates the prediction of domain-specific cognitive decline. This approach may help to increase the sensitivity to detect Alzheimer's disease-related cognitive decline and to determine personalized cognitive endpoints in clinical trials.

Identifiants

pubmed: 36345046
doi: 10.1186/s13195-022-01105-5
pii: 10.1186/s13195-022-01105-5
pmc: PMC9639286
doi:

Substances chimiques

tau Proteins 0
Amyloid 0
Amyloid beta-Peptides 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

166

Informations de copyright

© 2022. The Author(s).

Références

Brain. 2020 Apr 1;143(4):1249-1260
pubmed: 32176777
Acta Neuropathol. 1991;82(4):239-59
pubmed: 1759558
Alzheimers Dement (N Y). 2019 May 20;5:164-174
pubmed: 31193334
J Alzheimers Dis. 2021;80(3):1091-1104
pubmed: 33682705
Neurology. 2021 Jun 1;96(22):e2673-e2684
pubmed: 34550903
Neuron. 2016 Mar 2;89(5):971-982
pubmed: 26938442
J Neurosci. 2011 Nov 2;31(44):15775-86
pubmed: 22049421
Brain. 2018 May 1;141(5):1486-1500
pubmed: 29522171
JAMA Neurol. 2021 Aug 1;78(8):961-971
pubmed: 34180956
Cold Spring Harb Perspect Med. 2012 Apr;2(4):a006171
pubmed: 22474609
Alzheimers Dement. 2014 Nov;10(6):666-74
pubmed: 24751827
Alzheimers Dement. 2011 May;7(3):263-9
pubmed: 21514250
Nat Med. 2021 Jul;27(7):1187-1196
pubmed: 34155411
JAMA Neurol. 2015 Mar;72(3):316-24
pubmed: 25580592
Arch Neurol. 2007 Sep;64(9):1323-9
pubmed: 17846273
Alzheimers Dement. 2018 Apr;14(4):535-562
pubmed: 29653606
EMBO Mol Med. 2020 Sep 7;12(9):e12308
pubmed: 32790063
J Psychiatr Res. 1975 Nov;12(3):189-98
pubmed: 1202204
Brain. 2019 Jun 1;142(6):1723-1735
pubmed: 31009046
Mol Psychiatry. 2021 Oct;26(10):5888-5898
pubmed: 34593971
Alzheimers Dement. 2011 May;7(3):270-9
pubmed: 21514249
Lancet Neurol. 2021 Jun;20(6):484-496
pubmed: 33933186
Alzheimers Res Ther. 2018 Dec 19;10(1):122
pubmed: 30567585
Lancet Neurol. 2007 Aug;6(8):734-46
pubmed: 17616482
Brain. 2017 Dec 1;140(12):3286-3300
pubmed: 29053874
PLoS Comput Biol. 2017 Oct 23;13(10):e1005649
pubmed: 29059185
Brain. 2018 May 1;141(5):1517-1528
pubmed: 29538647
Brain Imaging Behav. 2012 Dec;6(4):502-16
pubmed: 22782295
Crit Care. 2016 Aug 03;20(1):218
pubmed: 27485596
JAMA Netw Open. 2020 Mar 2;3(3):e200413
pubmed: 32142126
Alzheimers Dement (Amst). 2018 Feb 23;10:232-236
pubmed: 29780868
Sci Adv. 2020 Nov 27;6(48):
pubmed: 33246962
Lancet Neurol. 2014 Jun;13(6):614-29
pubmed: 24849862
Brain. 2021 Oct 22;144(9):2771-2783
pubmed: 33725124
Curr Opin Neurobiol. 2011 Dec;21(6):929-34
pubmed: 22079495
Alzheimers Res Ther. 2021 Apr 17;13(1):80
pubmed: 33865446
JAMA Neurol. 2021 Apr 1;78(4):445-453
pubmed: 33587110
PLoS Comput Biol. 2011 Nov;7(11):e1002251
pubmed: 22072952
J Neurosci. 2017 Apr 19;37(16):4323-4331
pubmed: 28314821
Nat Neurosci. 2019 Jan;22(1):57-64
pubmed: 30559471
Neurobiol Aging. 2020 Aug;92:141-152
pubmed: 32280029
Alzheimers Res Ther. 2021 Aug 12;13(1):137
pubmed: 34384484
Alzheimers Dement (N Y). 2020 Dec 05;6(1):e12072
pubmed: 33313380
Brain. 2016 May;139(Pt 5):1551-67
pubmed: 26962052
Mol Psychiatry. 2019 Aug;24(8):1112-1134
pubmed: 30635637
Nat Commun. 2020 May 26;11(1):2612
pubmed: 32457389
Alzheimers Res Ther. 2018 Sep 11;10(1):90
pubmed: 30205840
Cereb Cortex. 2014 Jun;24(6):1422-35
pubmed: 23314940
Nat Med. 2021 May;27(5):871-881
pubmed: 33927414
Nat Methods. 2011 Jun 26;8(8):665-70
pubmed: 21706013

Auteurs

Davina Biel (D)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.

Ying Luan (Y)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.

Matthias Brendel (M)

Department of Nuclear Medicine, University Hospital, LMU Munich, Munich, Germany.

Paul Hager (P)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.

Anna Dewenter (A)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.

Alexis Moscoso (A)

Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Diana Otero Svaldi (D)

Eli Lilly and Company, Indianapolis, IN, USA.

Ixavier A Higgins (IA)

Eli Lilly and Company, Indianapolis, IN, USA.

Michael Pontecorvo (M)

Avid Radiopharmaceuticals, Philadelphia, PA, USA.

Sebastian Römer (S)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.
Department of Neurology, University Hospital, LMU Munich, Munich, Germany.

Anna Steward (A)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.

Anna Rubinski (A)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.

Lukai Zheng (L)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.

Michael Schöll (M)

Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.

Sergey Shcherbinin (S)

Eli Lilly and Company, Indianapolis, IN, USA.

Michael Ewers (M)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany.
German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.

Nicolai Franzmeier (N)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377, Munich, Germany. Nicolai.Franzmeier@med.uni-muenchen.de.
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Nicolai.Franzmeier@med.uni-muenchen.de.

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