Literature DB >> 32144983

Resting State Functional Connectivity Signature Differentiates Cognitively Normal from Individuals Who Convert to Symptomatic Alzheimer's Disease.

Julie K Wisch1, Catherine M Roe1,2, Ganesh M Babulal1,2, Suzanne E Schindler1,2, Anne M Fagan3,2, Tammie L Benzinger4,2, John C Morris1,4,2, Beau M Ances1,4,3,2.   

Abstract

BACKGROUND: Changes in resting state functional connectivity (rs-fc) occur in Alzheimer's disease (AD), but few longitudinal rs-fc studies have been performed. Most studies focus on single networks and not a global measure of rs-fc. Although the amyloid tau neurodegeneration (AT(N)) framework is increasingly utilized by the AD community, few studies investigated when global rs-fc signature changes occur within this model.
OBJECTIVE: 1) Identify a global rs-fc signature that differentiates cognitively normal (CN) individuals from symptomatic AD. 2) Assess when longitudinal changes in rs-fc occur relative to conversion to symptomatic AD. 3) Compare rs-fc with amyloid, tau, and neurodegeneration biomarkers.
METHODS: A global rs-fc signature composed of intra-network connections was longitudinally evaluated in a cohort of cognitively normal participants at baseline (n = 335). Biomarkers, including cerebrospinal fluid (Aβ42 and tau), structural magnetic resonance imaging, and positron emission tomography were obtained.
RESULTS: Global rs-fc signature distinguished CN individuals from individuals who developed symptomatic AD. Changes occurred nearly four years before conversion to symptomatic AD. The global rs-fc signature most strongly correlated with markers of neurodegeneration.
CONCLUSION: The global rs-fc signature changes near symptomatic onset and is likely a neurodegenerative biomarker. Rs-fc changes could serve as a biomarker for evaluating potential therapies for symptomatic conversion to AD.

Entities:  

Keywords:  Alzheimer’s disease; biomarkers; neuroimaging; observational studies

Mesh:

Substances:

Year:  2020        PMID: 32144983      PMCID: PMC7183885          DOI: 10.3233/JAD-191039

Source DB:  PubMed          Journal:  J Alzheimers Dis        ISSN: 1387-2877            Impact factor:   4.472


  41 in total

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