Aβ-induced vulnerability propagates via the brain’s default mode network

Tharick A. Pascoal, Sulantha Mathotaarachchi, Min Su Kang, Sara Mohaddes, Monica Shin, Ah Yeon Park, Maxime J. Parent, Andrea L. Benedet, Mira Chamoun, Joseph Therriault, Heungsun Hwang, A. Claudio Cuello, Bratislav Misic, Jean-Paul Soucy, John A. D. Aston, Serge Gauthier and Pedro Rosa-Neto ()
Additional contact information
Tharick A. Pascoal: The McGill University Research Centre for Studies in Aging
Sulantha Mathotaarachchi: The McGill University Research Centre for Studies in Aging
Min Su Kang: The McGill University Research Centre for Studies in Aging
Sara Mohaddes: The McGill University Research Centre for Studies in Aging
Monica Shin: The McGill University Research Centre for Studies in Aging
Ah Yeon Park: University of Cambridge
Maxime J. Parent: The McGill University Research Centre for Studies in Aging
Andrea L. Benedet: The McGill University Research Centre for Studies in Aging
Mira Chamoun: The McGill University Research Centre for Studies in Aging
Joseph Therriault: The McGill University Research Centre for Studies in Aging
Heungsun Hwang: McGill University
A. Claudio Cuello: McGill University
Bratislav Misic: Montreal Neurological Institute
Jean-Paul Soucy: Montreal Neurological Institute
John A. D. Aston: University of Cambridge
Serge Gauthier: The McGill University Research Centre for Studies in Aging
Pedro Rosa-Neto: The McGill University Research Centre for Studies in Aging

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: Abstract The link between brain amyloid-β (Aβ), metabolism, and dementia symptoms remains a pressing question in Alzheimer’s disease. Here, using positron emission tomography ([18F]florbetapir tracer for Aβ and [18F]FDG tracer for glucose metabolism) with a novel analytical framework, we found that Aβ aggregation within the brain’s default mode network leads to regional hypometabolism in distant but functionally connected brain regions. Moreover, we found that an interaction between this hypometabolism with overlapping Aβ aggregation is associated with subsequent cognitive decline. These results were also observed in transgenic Aβ rats that do not form neurofibrillary tangles, which support these findings as an independent mechanism of cognitive deterioration. These results suggest a model in which distant Aβ induces regional metabolic vulnerability, whereas the interaction between local Aβ with a vulnerable environment drives the clinical progression of dementia.

Date: 2019
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DOI: 10.1038/s41467-019-10217-w

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