1153 Associations Between Dim Light Melatonin Onset and Salience Network Functional Connectivity in Later-Life Adults

Abstract Introduction Disruptions in resting-state functional connectivity within the Salience Network (SN) and Default Mode Network (DMN), as well as their connectivity with the hippocampus, have been associated with cognitive decline and neurodegenerative disorders such as Alzheimer’s disease and related dementias. As people age, circadian timing tends to advance, and sleep becomes increasingly fragmented and disrupted, which may also exacerbate cognitive decline and elevate the risk of neurodegenerative conditions. However, there is limited research examining the association between circadian rhythms and functional connectivity in aging. This study examined how circadian timing is associated with alterations in functional connectivity within the SN and DMN, as well as hippocampal connectivity to these networks. Methods We analyzed data from 50 cognitively healthy later-life adults (mean age ± SD = 68 ± 6.50, female [n = 25 (52%)]). Dim light melatonin onset (DLMO) determined circadian timing. T1-weighted and BOLD images from 3.0T MRI data were collected. Correlation maps were generated by extracting the residual BOLD signal from the regions of interest (ROIs) and calculating Pearson correlation coefficients between that signal and the signals from all other voxels. These correlation values were then transformed into z-scores using Fisher’s transformation. Results Later DLMO was associated with higher SN strength (r = 0.37, p = 0.0079). However, DLMO was not correlated with DMN strengths, hippocampal-DMN connectivity, or hippocampal-SN connectivity. Conclusion Later circadian timing was significantly associated with higher SN strength, suggesting that clinicians can identify individuals at increased risk of neuronal changes associated with circadian disruption. Future studies with a larger sample, comprehensive covariates, and a prospective design are warranted to investigate this relationship further. Support (if any) Part of this work was supported by the University of Iowa Institute for Clinical and Translational Science (NIH/ ACTS KL2TR002536, PI: Bassuk, Scholar: Moon), University of Iowa Center for Advancing Multimorbidity Science (NIH/NINR P20 NR018081, MPI: Gardner & Rakel, Pilot PI: Moon), Alzheimer’s Association (AARG-19-618403, PI: Moon). This work was conducted on an MRI instrument funded by 1S10OD025025-01. Contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH/ACTS, NIH/NINR, or Alzheimer’s Association.