Impaired cerebral hemodynamics in late-onset depression: computed tomography angiography, computed tomography

Jinhong Wang1, Renren Li2, Meng Liu2

  • 1Department of Medical Imaging, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Insights

Late-onset depression (LOD) is linked to brain blood flow issues and white matter changes. Imaging biomarkers like middle cerebral artery stenosis and hypoperfusion can indicate cerebrovascular pathology in LOD.

Area of Science:

  • Neuroscience
  • Radiology
  • Psychiatry

Background:

  • Late-onset depression (LOD) presents diagnostic challenges, often lacking family history or severe psychopathology.
  • Cerebrovascular comorbidities and cerebral microvascular lesions are increasingly implicated in LOD development and progression.

Purpose of the Study:

  • To investigate the association between late-onset depression and macrovascular and microvascular brain changes.
  • To explore the pathomechanism and course of late-onset depression using multi-imaging techniques.

Main Methods:

  • 116 participants (LOD group and age/sex-matched controls) underwent evaluation.
  • Methods included CT angiography (CTA) for arterial stenosis, CT perfusion (CTP) for cerebral blood flow (CBF), and FLAIR MRI for white matter hyperintensities (WMH).
  • Cognitive/mood status and depression severity (Hamilton Depression Scale) were assessed.

Main Results:

  • Participants with LOD showed higher rates of intracranial arterial stenosis, particularly in the middle cerebral artery (MCA).
  • Significant global and regional cerebral hypoperfusion was observed in the LOD group, especially in frontal and parietal lobes.
  • Increased white matter hyperintensity (WMH) loads in deep white matter were significantly associated with LOD.

Conclusions:

  • Imaging biomarkers such as hypoperfusion, MCA stenosis, and high WMH loads can identify cerebrovascular pathology in LOD.
  • These findings suggest macrovascular and microvascular changes are key in the pathophysiology of late-onset depression.
Abstract

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