Decomposed arterial stiffness and NfL–cognition association in older adults: The IGNITE study
Amani M. Norling, Audrey M. Collins, Kelsey R. Sewell, Lu Wan, George Grove, Haiqing Huang, Timothy M. Hughes, Adam D. Gepner, Akira Sekikawa, Lauren E. Oberlin, Thomas K. Karikari, Jill K. Morris, John M. Jakicic, Renee J. Rogers, Daniel E. Forman, Edward McAuley, Arthur F. Kramer, Charles H. Hillman, Eric D. Vidoni, Sandra A. Billinger, Jeffrey M. Burns, Anna L. Marsland, Chaeryon Kang, Kirk I. EricksonAbstract
BACKGROUND
Neurofilament light chain (NfL) indexes neuroaxonal injury and relates to poorer cognition. Higher carotid–femoral pulse wave velocity (cfPWV) arterial stiffness strengthens NfL–cognition associations, but reflects both pressure‐standardized structural stiffness (S–PWV) and transient hemodynamic load‐dependent pulse wave velocity (LD–PWV). We tested which component drives this interaction.
METHODS
Plasma NfL and cfPWV were measured in 552 cognitively unimpaired older adults. cfPWV was decomposed into S–PWV and LD–PWV. Five latent cognitive domains were modeled. Linear regression tested PWV moderators of NfL–cognition associations.
RESULTS
NfL correlated with all domains ( r = −0.116 to −0.185; P < 0.01) and was unrelated to S–PWV or LD–PWV. Total–PWV moderated NfL–working memory (β = −0.268, P = 0.019). NfL × S–PWV interactions were significant for episodic memory, working memory, and processing speed ( P < 0.040), but did not meet false discovery rate correction ( q ≈ 0.067). NfL × LD–PWV interactions were non‐significant ( P > 0.09).
DISCUSSION
Nominal interactions were more consistent for S–PWV. Findings did not provide multiplicity‐adjusted evidence of component‐specific moderation.
ClinicalTrials.gov: NCT02875301