4.7 Article

The impact of demographic, clinical, genetic, and imaging variables on tau PET status

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SPRINGER
DOI: 10.1007/s00259-020-05099-w

关键词

PET; Tau; Aβ Alzheimer’ s disease; MCI; Dementia

资金

  1. Vrije Universiteit Amsterdam
  2. Swedish Research Council
  3. Knut and Alice Wallenberg foundation
  4. Marianne and Marcus Wallenberg foundation
  5. Strategic Research Area MultiPark (Multidisciplinary Research in Parkinson's disease) at Lund University
  6. Swedish Alzheimer Foundation
  7. Swedish Brain Foundation
  8. Medical Faculty at Lund University
  9. Region Skane
  10. Parkinson foundation of Sweden
  11. Parkinson Research Foundation
  12. Skane University Hospital Foundation
  13. Swedish federal government under the ALF agreement
  14. Alzheimer's Society Junior Fellowship [ASJF-17-011, P30AG062422, P01-AG019724, R01AG038791, R01-NS050915, K99 AG065501, R01 AG045611]
  15. Alzheimer's Association [AACSF-19-617663]
  16. Rainwater Charitable Foundation (GDR)
  17. GE Healthcare
  18. Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health) [U01 AG024904]
  19. DOD ADNI (Department of Defense) [W81XWH-12-2-0012]
  20. National Institute on Aging
  21. National Institute of Biomedical Imaging and Bioengineering
  22. Alzheimer's Drug Discovery Foundation
  23. Araclon Biotech
  24. Biogen
  25. Bristol-Myers Squibb Company
  26. CereSpir, Inc.
  27. Cogstate
  28. Elan Pharmaceuticals, Inc.
  29. Eli Lilly and Company
  30. EuroImmun
  31. F. Hoffmann-La Roche Ltd.
  32. Canadian Institutes of Health Research
  33. Fonds de Recherche du Quebec - Sante (FRQ-S)
  34. Pfizer Canada
  35. J. L. Levesque Foundation
  36. Lemaire Foundation
  37. Douglas Hospital Research Centre and Foundation
  38. Government of Canada
  39. Canada Fund for Innovation
  40. Alzheimer's Association Grant
  41. Alzheimer Society of Canada
  42. Canada Institutes of Health Research [PJT162091, PJT-148963]
  43. Bundy Academy
  44. AbbVie
  45. Alzheimer's Association
  46. BioClinica, Inc.
  47. Eisai Inc.
  48. McGill University

向作者/读者索取更多资源

The study revealed that age, MMSE score, and AD-signature cortical thickness were strongly associated with tau PET positivity in Alzheimer's disease and mild cognitive impairment patients with Aβ positivity, while the presence of Aβ was the strongest predictor of a positive tau PET scan in non-AD neurodegenerative disorder patients and cognitively unimpaired individuals.
Purpose A substantial proportion of amyloid-beta (A beta)+ patients with clinically diagnosed Alzheimer's disease (AD) dementia and mild cognitive impairment (MCI) are tau PET-negative, while some clinically diagnosed non-AD neurodegenerative disorder (non-AD) patients or cognitively unimpaired (CU) subjects are tau PET-positive. We investigated which demographic, clinical, genetic, and imaging variables contributed to tau PET status. Methods We included 2338 participants (430 A beta+ AD dementia, 381 A beta+ MCI, 370 non-AD, and 1157 CU) who underwent [F-18]flortaucipir (n = 1944) or [F-18]RO948 (n = 719) PET. Tau PET positivity was determined in the entorhinal cortex, temporal meta-ROI, and Braak V-VI regions using previously established cutoffs. We performed bivariate binary logistic regression models with tau PET status (positive/negative) as dependent variable and age, sex, APOE epsilon 4, A beta status (only in CU and non-AD analyses), MMSE, global white matter hyperintensities (WMH), and AD-signature cortical thickness as predictors. Additionally, we performed multivariable binary logistic regression models to account for all other predictors in the same model. Results Tau PET positivity in the temporal meta-ROI was 88.6% for AD dementia, 46.5% for MCI, 9.5% for non-AD, and 6.1% for CU. Among A beta+ participants with AD dementia and MCI, lower age, MMSE score, and AD-signature cortical thickness showed the strongest associations with tau PET positivity. In non-AD and CU participants, presence of A beta was the strongest predictor of a positive tau PET scan. Conclusion We identified several demographic, clinical, and neurobiological factors that are important to explain the variance in tau PET retention observed across the AD pathological continuum, non-AD neurodegenerative disorders, and cognitively unimpaired persons.

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