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 - Funding Information:
This study was funded by grants from the National Institutes of Health (R01AG027012 and R01AG057723 to Dr. Semba; and R01HL111271 and R21HL112662 to Dr. Ferrucci) and National Institute on Aging contract 263MD9164 (to Dr. Ferrucci) and was supported by the Intramural Research Program of the National Institute on Aging, National Institutes of Health. “The InCHIANTI study baseline (1998‐2000) was supported as a ‘targeted project' (ICS110.1/RF97.71) by the Italian Ministry of Health and in part by the U.S. National Institute on Aging (Contracts: 263 MD 9164 and 263 MD 821336); the InCHIANTI Follow‐up 1 (2001‐2003) was funded by the U.S. National Institute on Aging (Contracts: N.1‐AG‐1‐1 and N.1‐AG‐1‐2111); and the InCHIANTI Follow‐ups 2 and 3 studies (2004‐2010) were financed by the U.S. National Institute on Aging (Contract: N01‐AG‐5‐0002) and supported in part by the Intramural Research Program of the National Institute on Aging, National Institutes of Health, Baltimore, Maryland.”
Funding Information:
This study was funded by grants from the National Institutes of Health (R01AG027012 and R01AG057723 to Dr. Semba; and R01HL111271 and R21HL112662 to Dr. Ferrucci) and National Institute on Aging contract 263MD9164 (to Dr. Ferrucci) and was supported by the Intramural Research Program of the National Institute on Aging, National Institutes of Health. “The InCHIANTI study baseline (1998-2000) was supported as a ‘targeted project' (ICS110.1/RF97.71) by the Italian Ministry of Health and in part by the U.S. National Institute on Aging (Contracts: 263 MD 9164 and 263 MD 821336); the InCHIANTI Follow-up 1 (2001-2003) was funded by the U.S. National Institute on Aging (Contracts: N.1-AG-1-1 and N.1-AG-1-2111); and the InCHIANTI Follow-ups 2 and 3 studies (2004-2010) were financed by the U.S. National Institute on Aging (Contract: N01-AG-5-0002) and supported in part by the Intramural Research Program of the National Institute on Aging, National Institutes of Health, Baltimore, Maryland.”
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 -