4.8 Article

Basal forebrain degeneration precedes and predicts the cortical spread of Alzheimer's pathology

Journal

NATURE COMMUNICATIONS
Volume 7, Issue -, Pages -

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms13249

Keywords

-

Funding

  1. Alzheimer's Association grant [NIRG-14-320049]
  2. Alzheimer's Disease
  3. ADNI (National Institutes of Health Grant) [U01 AG024904]
  4. DOD ADNI (Department of Defense award) [W81XWH-12-2-0012]
  5. National Institute on Aging
  6. National Institute of Biomedical Imaging and Bioengineering
  7. AbbVie
  8. Alzheimer's Association
  9. Alzheimer's Drug Discovery Foundation
  10. Araclon Biotech
  11. BioClinica, Inc.
  12. Biogen
  13. Bristol-Myers Squibb Company
  14. CereSpir, Inc.
  15. Eisai Inc.
  16. Elan Pharmaceuticals, Inc.
  17. Eli Lilly and Company
  18. EuroImmun
  19. F. Hoffmann-La Roche Ltd
  20. Genentech, Inc.
  21. Fujirebio
  22. GE Healthcare
  23. IXICO Ltd
  24. Janssen Alzheimer Immunotherapy Research and Development, LLC
  25. Johnson & Johnson Pharmaceutical Research and Development LLC
  26. Lumosity
  27. Lundbeck
  28. Merck Co., Inc.
  29. Meso Scale Diagnostics, LLC
  30. NeuroRx Research
  31. Neurotrack Technologies
  32. Novartis Pharmaceuticals Corporation
  33. Pfizer, Inc.
  34. Piramal Imaging
  35. Servier
  36. Takeda Pharmaceutical Company
  37. Transition Therapeutics
  38. Canadian Institutes of Health Research

Ask authors/readers for more resources

There is considerable debate whether Alzheimer's disease (AD) originates in basal forebrain or entorhinal cortex. Here we examined whether longitudinal decreases in basal forebrain and entorhinal cortex grey matter volume were interdependent and sequential. In a large cohort of age-matched older adults ranging from cognitively normal to AD, we demonstrate that basal forebrain volume predicts longitudinal entorhinal degeneration. Models of parallel degeneration or entorhinal origin received negligible support. We then integrated volumetric measures with an amyloid biomarker sensitive to pre-symptomatic AD pathology. Comparison between cognitively matched normal adult subgroups, delineated according to the amyloid biomarker, revealed abnormal degeneration in basal forebrain, but not entorhinal cortex. Abnormal degeneration in both basal forebrain and entorhinal cortex was only observed among prodromal (mildly amnestic) individuals. We provide evidence that basal forebrain pathology precedes and predicts both entorhinal pathology and memory impairment, challenging the widely held belief that AD has a cortical origin.

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