TY - JOUR
T1 - Plasma proteomic signature of the risk of developing mobility disability
T2 - A 9-year follow-up
AU - Osawa, Yusuke
AU - Semba, Richard D.
AU - Fantoni, Giovanna
AU - Candia, Julián
AU - Biancotto, Angélique
AU - Tanaka, Toshiko
AU - Bandinelli, Stefania
AU - Ferrucci, Luigi
N1 - Publisher Copyright:
© 2020 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
PY - 2020/4/1
Y1 - 2020/4/1
N2 - Introduction: Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data-driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community-dwelling older adults without mobility disability at baseline. Methods: We investigated 660 women and men, aged 71.9 ± 6.0 (60–94) years, who participated in the Invecchiare in Chianti, “Aging in the Chianti Area” study and completed the 400-m walk at fast pace (400-m walk) at enrollment. Median follow-up time was 8.57 [interquartile, 3.20–9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400-m walk. Protein-specific Cox proportional hazard model was adjusted for sex, age, and other important covariates. Results: Plasma levels of 75 proteins predicted mobility disability (p '.05). Significant proteins were enriched for the KEGG “PI3K-Akt signaling,” “phagosomes,” and “cytokine–cytokine receptor interaction” pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin-2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility. Conclusion: CTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community-dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability.
AB - Introduction: Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data-driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community-dwelling older adults without mobility disability at baseline. Methods: We investigated 660 women and men, aged 71.9 ± 6.0 (60–94) years, who participated in the Invecchiare in Chianti, “Aging in the Chianti Area” study and completed the 400-m walk at fast pace (400-m walk) at enrollment. Median follow-up time was 8.57 [interquartile, 3.20–9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400-m walk. Protein-specific Cox proportional hazard model was adjusted for sex, age, and other important covariates. Results: Plasma levels of 75 proteins predicted mobility disability (p '.05). Significant proteins were enriched for the KEGG “PI3K-Akt signaling,” “phagosomes,” and “cytokine–cytokine receptor interaction” pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin-2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility. Conclusion: CTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community-dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability.
KW - cathepsin S
KW - growth/differentiation factor 15
KW - mobility disability
KW - proteomics
KW - thrombospondin-2
UR - http://www.scopus.com/inward/record.url?scp=85081222242&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85081222242&partnerID=8YFLogxK
U2 - 10.1111/acel.13132
DO - 10.1111/acel.13132
M3 - Article
C2 - 32157804
AN - SCOPUS:85081222242
SN - 1474-9718
VL - 19
JO - Aging Cell
JF - Aging Cell
IS - 4
M1 - e13132
ER -