ArticleNature communications2026
The default mode network exhibits circuit-specific selective vulnerability despite widespread amyloid burden in an animal model of Alzheimer's disease.
Samuel J Brunwasser, James N McGregor, Kiran Bhaskaran-Nair, Clayton A Farris, Halla Elmore, Bryan T Higashikubo, Zachary D Berriman-Rozen, Dongjun Ko, Eva L Dyer, John M Grady and 3 more
Abstract read
In one paragraphArticle in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 · Who and what moneyAuthors and funding
13 authors.
Samuel J Brunwasser *Department of Biology, Washington University in St. Louis, St. Louis, MO, USA.
James N McGregor *Department of Biology, Washington University in St. Louis, St. Louis, MO, USA.
Kiran Bhaskaran-NairDepartment of Biology, Washington University in St. Louis, St. Louis, MO, USA.
Clayton A FarrisDepartment of Biology, Washington University in St. Louis, St. Louis, MO, USA.
Bryan T HigashikuboDepartment of Biology, Washington University in St. Louis, St. Louis, MO, USA.
Zachary D Berriman-RozenDepartment of Biology, Washington University in St. Louis, St. Louis, MO, USA.ORCID 0009-0004-0452-8432 Dongjun KoDepartment of Biology, Washington University in St. Louis, St. Louis, MO, USA.
Eva L DyerDepartment of Computer & Information Science, University of Pennsylvania, Philadelphia, PA, USA.ORCID 0000-0002-6962-524X John M GradyDepartment of Biology, Washington University in St. Louis, St. Louis, MO, USA.
Jennifer D WhitesellAllen Institute for Brain Science, Seattle, WA, USA.
Julie A HarrisAllen Institute for Brain Science, Seattle, WA, USA.
Keith B HengenDepartment of Biology, Washington University in St. Louis, St. Louis, MO, USA. khengen@wustl.edu.ORCID 0000-0001-5017-4090 Funding
Mouse Cell Type-Specific Brain Mapping in Health and DiseaseR01AG047589 · NIA · ALLEN INSTITUTE · PI HARRIS, JULIE · 2014 to 2018
$3.4MA Comparative Framework for Modeling the Low-Dimensional Geometry of Neural Population StatesR01EB029852 · NIBIB · GEORGIA INSTITUTE OF TECHNOLOGY · PI DYER, EVA · 2020 to 2020
$1.1MRobust circuit computation in freely behaving animals.R01NS118442 · NINDS · WASHINGTON UNIVERSITY · PI HENGEN, KEITH B. · 2023 to 2024
$1.0MSleep reinforces homeostatic set-points in neural activity and mitigates neurodegenerative diseaseR01AG091773 · NIA · WASHINGTON UNIVERSITY · PI Keith B. Hengen · 2026 to 2026
$579kBrightFocus Foundation (BrightFocus) A2022038SNIA NIH HHS R01 AG047589NIA NIH HHS R01 AG091773NIBIB NIH HHS R01 EB029852NINDS NIH HHS R01 NS118442U.S. Department of Health & Human Services | National Institutes of Health (NIH) 1R01EB029852U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01AG091773U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) R01AG047589
6 · The paper itselfAbstract
In Alzheimer's Disease (AD) the default mode network (DMN) exhibits selective vulnerability to functional decline and amyloid beta (Aβ) plaques in early AD. DMN vulnerability may simply be the result of Aβ accumulation. Alternately, Aβ may unmask an intrinsic susceptibility of DMN circuits. Should DMN vulnerability persist amidst global Aβ deposition, this would support the latter hypothesis. We tested this using long-term, multi-region recordings of single units in mice characterized by widespread Aβ (APP/PS1). We tracked a neuronal population within the retrosplenial cortex (a DMN region) and two monosynaptically connected target populations, one within (anterior cingulate) and the other outside the DMN (primary visual cortex). We also recorded in hippocampus and examined interactions between the in-DMN and out-DMN circuits. Our data revealed progressive dysfunction restricted to the in-DMN circuit. In contrast, communication originating within but targeting an out-DMN population was unaffected by disease. Dysfunction was pronounced in sleep.
Indexed as
Alzheimer DiseaseAmyloid beta-PeptidesDefault Mode NetworkNerve NetAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalFemaleGyrus CinguliHippocampusMaleMiceMice, TransgenicNeuronsPlaque, AmyloidAmyloid beta-PeptidesAmyloid beta-Protein Precursor
Identifiers
PMID42816467
PMCPMC13627688
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