Cerebral vascular burden on hippocampal subfields in first-onset drug-naïve subjects with late-onset depression

- This study is the first to elaborate distinctive association patterns between hippocampal subfield volumes and cerebral vascular burden in LOD.
- White matter hyperintensity was negatively correlated with left total hippocampal volume and CA1 in the LOD group.
- In addition, depression severity was negatively associated with left and right CA3 volumes in the LOD group.

BackgroundAlthough there is substantial evidence of associations between frontal-striatal circuits and cerebral vascular burden in late-onset depression (LOD), relationships between vascular burden and hippocampal subfields are not clear. The purpose of this study was to investigate relationships between cerebral vascular burden and hippocampal subfield volume in LOD patients.MethodsFifty subjects with LOD and 50 group-matched healthy control subjects underwent magnetic resonance imaging scanning. Hippocampal subfields volumes were measured and compared between the groups. In addition, association patterns between white matter hyperintensity (WMH) volumes, clinical measures and hippocampal subfield volumes were investigated in the LOD group.ResultsSubjects with LOD exhibited significant hippocampal volume reductions in the total hippocampus, cornu ammonis (CA) 1 and 3 and dentate gyrus (DG) areas compared with healthy subjects. Total WMH volume was negatively correlated with left total hippocampal volume and CA1 in the LOD group. In addition, depression severity was negatively associated with left and right CA3 volumes in the LOD group.LimitationOur findings of distinctive relationships between WMH and hippocampal subfields demonstrate a simple correlation, but do not prove causationConclusionThis study is the first to elaborate distinctive association patterns between hippocampal subfield volumes and cerebral vascular burden in LOD. These structural changes in the hippocampal CA1, CA3 and DG areas might be at the core of the underlying neurobiological mechanisms of hippocampal dysfunction in LOD. However, longitudinal studies will be needed to identify the mechanisms of these structural changes.