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Relationship between severe amyloid angiopathy, apolipoprotein E genotype, and vascular lesions in Alzheimer's

J M Olichney1, L A Hansen, J H Lee

  • 1Alzheimer's Disease Research Center, University of California, San Diego, La Jolla, California 92093-0948, USA. olichney@cogsci.ucsd.edu

Annals of the New York Academy of Sciences
|May 20, 2000
PubMed

Insights

Cerebral amyloid angiopathy (CAA) is linked to cerebrovascular lesions (VLs) in Alzheimer's disease (AD). Severe CAA contributes to VLs independently of apolipoprotein E (ApoE) genotype, suggesting a direct pathogenic role.

Area of Science:

  • Neurology
  • Neuroscience
  • Pathology

Background:

  • Cerebral amyloid angiopathy (CAA) is a significant factor in Alzheimer's disease (AD) pathology.
  • CAA is associated with various cerebrovascular lesions (VLs), including lobar hemorrhages, small infarcts, and microinfarcts.
  • Apolipoprotein E4 (ApoE4) is a major genetic risk factor for AD and may predispose individuals to CAA and cerebrovascular disease.

Purpose of the Study:

  • To elucidate the intricate relationship between CAA, ApoE, and VLs in AD.
  • To review evidence supporting CAA as a cause of specific VLs.
  • To examine the role of ApoE4 in CAA and cerebrovascular disease.

Main Methods:

  • Review of existing scientific literature and evidence.
  • Analysis of patient data stratified by ApoE genotype.
  • Examination of the association between CAA severity and VLs.

Main Results:

  • CAA is strongly associated with and may cause lobar hemorrhages, small infarcts, and microinfarcts.
  • ApoE4 influences susceptibility to CAA and cerebrovascular disease.
  • VLs increase with severe CAA, even within homogenous ApoE genotype groups (E4/4 and E3/3).

Conclusions:

  • The link between CAA and VLs is not solely due to ApoE genotype variations.
  • Severe CAA plays a direct pathogenic role in the development of many VLs observed in AD.
  • Understanding this relationship is crucial for AD pathogenesis and therapeutic strategies.

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