Central autonomic network dysfunction and plasma Alzheimer's disease biomarkers in older adults.


Journal

Alzheimer's research & therapy
ISSN: 1758-9193
Titre abrégé: Alzheimers Res Ther
Pays: England
ID NLM: 101511643

Informations de publication

Date de publication:
08 Jun 2024
Historique:
received: 22 03 2024
accepted: 24 05 2024
medline: 9 6 2024
pubmed: 9 6 2024
entrez: 8 6 2024
Statut: epublish

Résumé

Higher order regulation of autonomic function is maintained by the coordinated activity of specific cortical and subcortical brain regions, collectively referred to as the central autonomic network (CAN). Autonomic changes are frequently observed in Alzheimer's disease (AD) and dementia, but no studies to date have investigated whether plasma AD biomarkers are associated with CAN functional connectivity changes in at risk older adults. Independently living older adults (N = 122) without major neurological or psychiatric disorder were recruited from the community. Participants underwent resting-state brain fMRI and a CAN network derived from a voxel-based meta-analysis was applied for overall, sympathetic, and parasympathetic CAN connectivity using the CONN Functional Toolbox. Sensorimotor network connectivity was studied as a negative control. Plasma levels of amyloid (Aβ All autonomic networks were positively associated with Aβ The present study findings suggest that CAN function is associated with plasma AD biomarker levels. Specifically, lower CAN functional connectivity is associated with decreased plasma Aβ

Sections du résumé

BACKGROUND BACKGROUND
Higher order regulation of autonomic function is maintained by the coordinated activity of specific cortical and subcortical brain regions, collectively referred to as the central autonomic network (CAN). Autonomic changes are frequently observed in Alzheimer's disease (AD) and dementia, but no studies to date have investigated whether plasma AD biomarkers are associated with CAN functional connectivity changes in at risk older adults.
METHODS METHODS
Independently living older adults (N = 122) without major neurological or psychiatric disorder were recruited from the community. Participants underwent resting-state brain fMRI and a CAN network derived from a voxel-based meta-analysis was applied for overall, sympathetic, and parasympathetic CAN connectivity using the CONN Functional Toolbox. Sensorimotor network connectivity was studied as a negative control. Plasma levels of amyloid (Aβ
RESULTS RESULTS
All autonomic networks were positively associated with Aβ
CONCLUSION CONCLUSIONS
The present study findings suggest that CAN function is associated with plasma AD biomarker levels. Specifically, lower CAN functional connectivity is associated with decreased plasma Aβ

Identifiants

pubmed: 38851772
doi: 10.1186/s13195-024-01486-9
pii: 10.1186/s13195-024-01486-9
doi:

Substances chimiques

Biomarkers 0
Amyloid beta-Peptides 0
Peptide Fragments 0
amyloid beta-protein (1-42) 0
Glial Fibrillary Acidic Protein 0
Neurofilament Proteins 0
amyloid beta-protein (1-40) 0
neurofilament protein L 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

124

Subventions

Organisme : CIHR
ID : DFD-170763
Pays : Canada
Organisme : NIH HHS
ID : K24AG081325
Pays : United States
Organisme : NIH HHS
ID : P30AG066519
Pays : United States
Organisme : NIH HHS
ID : R01AG064228
Pays : United States

Informations de copyright

© 2024. The Author(s).

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Auteurs

Trevor Lohman (T)

University of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA.

Arunima Kapoor (A)

Department of Psychological Science, University of California, Irvine, Irvine, CA, USA.

Allison C Engstrom (AC)

Department of Psychological Science, University of California, Irvine, Irvine, CA, USA.

Fatemah Shenasa (F)

Department of Psychological Science, University of California, Irvine, Irvine, CA, USA.

John Paul M Alitin (JPM)

University of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA.

Aimee Gaubert (A)

University of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA.

Kathleen E Rodgers (KE)

Center for Innovations in Brain Science, Department of Pharmacology, University of Arizona, Tucson, AZ, USA.

David Bradford (D)

Center for Innovations in Brain Science, Department of Pharmacology, University of Arizona, Tucson, AZ, USA.

Mara Mather (M)

University of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA.

S Duke Han (SD)

Department of Psychology, University of Southern California, Los Angeles, CA, USA.

Elizabeth Head (E)

Department of Pathology and Laboratory Medicine, University of California, Irvine, Irvine, CA, USA.

Lorena Sordo (L)

Department of Pathology and Laboratory Medicine, University of California, Irvine, Irvine, CA, USA.

Julian F Thayer (JF)

Department of Psychological Science, University of California, Irvine, Irvine, CA, USA.

Daniel A Nation (DA)

University of Southern California, Leonard Davis School of Gerontology, Los Angeles, CA, USA. danation@usc.edu.
Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. danation@usc.edu.

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