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Subclinical cardiovascular remodeling, indicated by increased left ventricular (LV) mass index, is linked to neuroaxonal degeneration in individuals with mild cognitive impairment (MCI) and APOE-ε4 carriers, impacting white matter integrity.

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Area of Science:

  • Cardiovascular health and aging
  • Neurodegenerative disease research
  • Biomarker discovery in aging

Background:

  • Left ventricular (LV) mass index, a marker of subclinical cardiac remodeling, is associated with white matter damage in aging.
  • The molecular pathways linking LV mass index to white matter damage remain largely unknown.
  • Investigating cerebrospinal fluid (CSF) biomarkers may elucidate these pathways.

Purpose of the Study:

  • To assess the relationship between LV mass index and CSF biomarkers of microglial activation (sTREM2), axonal injury (NFL), neurodegeneration (total-tau), and amyloid-β.
  • To determine if these biomarkers mediate the association between LV mass index and white matter damage.
  • To explore interactions with mild cognitive impairment (MCI) and APOE-ε4 status.

Main Methods:

  • Analysis of 142 participants from the Vanderbilt Memory and Aging Project.
  • Cardiac MRI, lumbar puncture for CSF biomarkers, and diffusion tensor imaging were performed.
  • Linear regressions and voxel-wise analyses examined associations and mediation effects.

Main Results:

  • LV mass index was not directly associated with CSF biomarkers across all participants.
  • LV mass index showed a significant association with neurofilament light (NFL) in participants with MCI and APOE-ε4 carriers.
  • NFL partially mediated the relationship between LV mass index and white matter damage (up to 13%).

Conclusions:

  • Subclinical cardiac remodeling (increased LV mass index) is associated with neuroaxonal degeneration in individuals with MCI and APOE-ε4.
  • Neuroaxonal degeneration, indicated by NFL, partially explains the link between LV mass index and white matter damage.
  • Findings suggest neuroaxonal degeneration is a key pathway, rather than amyloid or microglial activation, in the relationship between cardiac remodeling and brain white matter damage.