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Cerebral amyloid angiopathy and vessel dysfunction

Steven M Greenberg1

  • 1Department of Neurology, Massachusetts General Hospital, Boston, Mass 02114, USA. greenberg@helix.mgh.harvard.edu

Cerebrovascular Diseases (Basel, Switzerland)
|March 20, 2002
PubMed

Insights

Cerebral amyloid angiopathy (CAA) contributes to hemorrhagic stroke and may also cause vessel dysfunction, reduced cerebral blood flow, and ischemia. Beta-amyloid deposition in brain vessels is a key factor in these effects.

Area of Science:

  • Neurology
  • Vascular Biology
  • Neurodegenerative Diseases

Background:

  • Cerebral amyloid angiopathy (CAA) is characterized by beta-amyloid peptide deposition in cerebral and meningeal vessels.
  • CAA is a known cause of hemorrhagic stroke.
  • Emerging evidence suggests CAA also contributes to cerebrovascular dysfunction and ischemia.

Purpose of the Study:

  • To review the evidence linking CAA to vessel dysfunction, reduced cerebral blood flow, and ischemia.
  • To discuss the role of beta-amyloid in these pathological processes.
  • To explore the clinical significance of vascular beta-amyloid in dementia.

Main Methods:

  • Literature review of studies on cerebral amyloid angiopathy.
  • Analysis of clinical data from hereditary and sporadic CAA cases.
  • Examination of findings from transgenic mouse models of CAA.

Main Results:

  • Accumulating evidence supports CAA's role in causing vessel dysfunction, reduced cerebral blood flow, and ischemic lesions.
  • Ischemic lesions are observed in hereditary CAA syndromes and some sporadic CAA patients.
  • Transgenic mouse data suggest mechanisms by which beta-amyloid impacts vessel physiology.

Conclusions:

  • CAA is implicated not only in hemorrhagic stroke but also in cerebrovascular dysfunction and ischemia.
  • Beta-amyloid deposition in cerebral vessels plays a critical role in these pathologies.
  • Vascular beta-amyloid represents a potential therapeutic target for dementia.

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