Mixed-location cerebral microbleeds as a biomarker of neurodegeneration in a memory clinic population

Bibek Gyanwali1,2, Muhammad Amin Shaik3, Chuen Seng Tan4

  • 1Memory Aging and Cognition Centre, National University Health System, Singapore.

Aging
|November 27, 2019
PubMed

Insights

Mixed-location cerebral microbleeds (CMBs) are linked to neurodegeneration, specifically reduced limbic cortical thickness and accumbens volume. Strictly lobar CMBs correlate with decreased white matter volume, suggesting distinct roles in brain atrophy.

Area of Science:

  • Neurology
  • Neuroimaging
  • Vascular Neurology

Background:

  • Cerebral microbleeds (CMBs) are associated with distinct pathologies based on location: lobar CMBs with cerebral amyloid angiopathy and deep CMBs with hypertensive arteriopathy.
  • The neurodegenerative impact of mixed-location CMBs remains largely uncharacterized.

Purpose of the Study:

  • To investigate the associations between strictly lobar, strictly deep, and mixed-location CMBs with markers of neurodegeneration, including cerebral atrophy.

Main Methods:

  • Recruited 477 memory clinic patients who underwent 3T MRI scans.
  • Categorized CMBs into strictly lobar, strictly deep, and mixed-location groups.
  • Quantified brain structures (cortical thickness, white matter volume, subcortical volumes) using Free-Surfer and analyzed associations with linear regression models.

Main Results:

  • Mixed-location CMBs showed significant associations with reduced limbic cortical thickness (β= -0.01) and smaller accumbens (β= -0.01) and hippocampal presubiculum volumes (β= -0.01).
  • Strictly lobar CMBs were associated with reduced total white matter volume (β= -0.03) and region-specific white matter volumes.

Conclusions:

  • Mixed-location CMBs are linked to specific patterns of neurodegeneration in limbic and subcortical regions.
  • Strictly lobar CMBs are associated with more widespread white matter atrophy.
  • Further research is needed to elucidate the underlying mechanisms, potentially involving shared pathways of vascular dysfunction and neurodegeneration.

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