Distinctive Clinical Effects of Haemorrhagic Markers in Cerebral Amyloid Angiopathy

Young Kyoung Jang1,2, Hee Jin Kim1,2, Jin San Lee3

  • 1Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Gangnam-gu, Seoul, 06351, Korea.

Scientific Reports
|November 24, 2017
PubMed

Insights

Restricted lobar cerebral microbleeds (CMBs) and cortical superficial siderosis (CSS) in cerebral amyloid angiopathy (CAA) are linked to distinct patterns of brain thinning and cognitive deficits, offering new insights into disease mechanisms.

Area of Science:

  • Neurology
  • Neuroimaging
  • Gerontology

Background:

  • Cerebral amyloid angiopathy (CAA) is characterized by amyloid-beta deposition in cerebral vasculature.
  • Restricted lobar cerebral microbleeds (CMBs) and cortical superficial siderosis (CSS) are key imaging markers of CAA.
  • The clinical implications of CMBs and CSS in CAA remain incompletely understood.

Purpose of the Study:

  • To investigate the clinical significance of CMBs and CSS in patients with clinically and radiologically diagnosed CAA.
  • To determine the association between these markers and cognitive function.
  • To explore the relationship between these markers, cortical thinning, and cognitive impairment.

Main Methods:

  • A cohort of 372 patients with possible or probable CAA was recruited.
  • Cortical thickness was assessed using surface-based neuroimaging methods.
  • Statistical analyses were performed to evaluate associations between CMBs, CSS, cortical thinning, and cognitive performance.

Main Results:

  • Restricted multiple lobar CMBs correlated with widespread cortical thinning.
  • CSS was associated with cortical thinning predominantly in the frontal regions.
  • CMBs impacted all cognitive domains, while CSS affected attention and frontal executive functions, with partial mediation by cortical thinning.

Conclusions:

  • Restricted lobar CMBs and CSS are associated with distinct patterns of cortical thinning and cognitive dysfunction in CAA.
  • These findings provide novel insights into the pathophysiological mechanisms underlying CAA.
  • Targeting these specific pathological features may offer potential therapeutic avenues for CAA patients.

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