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

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  • Taylor W. Schmitz

    (Medical Research Council, Cognition and Brain Sciences Unit
    Wolfson College, University of Cambridge)

  • R. Nathan Spreng

    (Laboratory of Brain and Cognition, Human Neuroscience Institute, Cornell University)

Abstract

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.

Suggested Citation

  • Taylor W. Schmitz & R. Nathan Spreng, 2016. "Basal forebrain degeneration precedes and predicts the cortical spread of Alzheimer’s pathology," Nature Communications, Nature, vol. 7(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13249
    DOI: 10.1038/ncomms13249
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    Cited by:

    1. Md Habibur Rahman & Silong Peng & Xiyuan Hu & Chen Chen & Md Rezanur Rahman & Shahadat Uddin & Julian M.W. Quinn & Mohammad Ali Moni, 2020. "A Network-Based Bioinformatics Approach to Identify Molecular Biomarkers for Type 2 Diabetes that Are Linked to the Progression of Neurological Diseases," IJERPH, MDPI, vol. 17(3), pages 1-25, February.
    2. Alfie Wearn & Stéfanie A. Tremblay & Christine L. Tardif & Ilana R. Leppert & Claudine J. Gauthier & Giulia Baracchini & Colleen Hughes & Patrick Hewan & Jennifer Tremblay-Mercier & Pedro Rosa-Neto & , 2024. "Neuromodulatory subcortical nucleus integrity is associated with white matter microstructure, tauopathy and APOE status," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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