eprintid: 10200748
rev_number: 9
eprint_status: archive
userid: 699
dir: disk0/10/20/07/48
datestamp: 2024-11-27 12:10:49
lastmod: 2024-11-27 12:10:49
status_changed: 2024-11-27 12:10:49
type: article
metadata_visibility: show
sword_depositor: 699
creators_name: Gong, Jessica
creators_name: Preminger, Zohar
creators_name: Steptoe, Andrew
creators_name: Fancourt, Daisy
title: Protein signatures associated with loneliness and social isolation: Plasma proteome analyses in the English Longitudinal Study of Ageing, with causal evidence from Mendelian randomization
ispublished: pub
divisions: UCL
divisions: B02
divisions: D12
divisions: G19
keywords: Social isolation; Loneliness; 
Proteomics; Mendelian randomization; 
Ageing
note: Copyright © 2024 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
abstract: Introduction:
The understanding of biological pathways related to loneliness and social isolation remains incomplete. Cutting-edge population-based proteomics offers opportunities to uncover novel biological pathways linked to social deficits.
//
Methods:
This study employed a proteome-wide and data-driven approach to estimate the cross-sectional associations between objective measures of social connections (i.e., social isolation) and subjective measures (i.e., loneliness) with protein abundance, using the English Longitudinal Study of Ageing.
//
Results:
Greater social isolation was associated with higher levels of 11 proteins (TNFRSF10A, MMP12, TRAIL-R2, SKR3, TNFRSF11A, VSIG2, PRSS8, FGFR2, KIM1, REN, and NEFL) after minimal adjustments; and three proteins were significantly associated after full adjustments (TNFRSF10A, TNFRSF11A, and HAOX1). Findings from two-sample Mendelian randomization indicated that a lower frequency of in-person social contact with friends or family causally increased levels of TNFRSF10A, TRAIL-R2, TNFRSF11A, and KIM1, and decreased the level of NEFL. The study also highlighted several enriched biological pathways, including necrosis and cell death regulation, dimerization of procaspase-8, and inhibition of caspase-8 pathways, which have previously not been linked to social deficits.
//
Conclusion:
These findings could help explain the relationship between social deficits and disease, confirming the importance of continuing to explore novel biological pathways associated with social deficits.
date: 2025-02
date_type: published
publisher: Elsevier BV
official_url: http://dx.doi.org/10.1016/j.bbi.2024.11.024
oa_status: green
full_text_type: pub
language: eng
primo: open
primo_central: open_green
verified: verified_manual
elements_id: 2338921
doi: 10.1016/j.bbi.2024.11.024
lyricists_name: Gong, Jessica
lyricists_id: JGONA20
actors_name: Gong, Jessica
actors_id: JGONA20
actors_role: owner
full_text_status: public
publication: Brain, Behavior, and Immunity
volume: 124
pagerange: 85-94
issn: 0889-1591
citation:        Gong, Jessica;    Preminger, Zohar;    Steptoe, Andrew;    Fancourt, Daisy;      (2025)    Protein signatures associated with loneliness and social isolation: Plasma proteome analyses in the English Longitudinal Study of Ageing, with causal evidence from Mendelian randomization.                   Brain, Behavior, and Immunity , 124    pp. 85-94.    10.1016/j.bbi.2024.11.024 <https://doi.org/10.1016/j.bbi.2024.11.024>.       Green open access   
 
document_url: https://discovery.ucl.ac.uk/id/eprint/10200748/1/Gong_1-s2.0-S0889159124007062-main.pdf