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Inherited and Acquired Decrease in Complement Receptor 1 (CR1) Density on Red Blood Cells Associated with High Levels

Rachid Mahmoudi1,2, Sarah Feldman3,4, Aymric Kisserli5,6

  • 1Department of Internal Medicine and Geriatrics, Reims University Hospitals, Maison Blanche Hospital, 45 rue cognac Jay, 51092 Reims, France. rmahmoudi@chu-reims.fr.

International Journal of Molecular Sciences
|July 26, 2018
PubMed

Insights

Alzheimer's disease (AD) is linked to lower complement receptor 1 (CR1) density on red blood cells, which may be acquired, not just inherited. This CR1 deficiency could impair amyloid clearance in AD.

Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • The complement receptor 1 (CR1) gene is implicated in Alzheimer's disease (AD) pathogenesis.
  • Previous research indicated AD is associated with reduced density of the long CR1 isoform, CR1*2 (S).

Purpose of the Study:

  • To correlate CR1 phenotype data (CR1 density per erythrocyte (CR1/E), soluble CR1 (sCR1)) with CR1 genetic data (polymorphisms) in AD patients and healthy controls.
  • To investigate the role of CR1 in AD pathogenesis and explore potential therapeutic targets.

Main Methods:

  • CR1/E enumeration via flow cytometry and sCR1 quantification by ELISA.
  • CR1 polymorphisms assessed using restriction fragment length polymorphism (RFLP), pyrosequencing, and high-resolution melting PCR.
  • Multivariate analysis to determine associations between CR1 density, genetic factors, and methylation.

Main Results:

  • AD patients with specific CR1 alleles (H or Q) exhibited significantly lower CR1/E compared to controls with the same alleles.
  • AD patients showed significantly higher levels of sCR1 compared to controls.
  • A reduction in CR1/E density was associated with increased CR1 methylation, suggesting acquired factors contribute to low CR1/E.

Conclusions:

  • Low CR1/E density in AD is influenced by both inherited genetic factors and acquired epigenetic modifications.
  • CR1's role in AD pathogenesis may involve impaired clearance of amyloid deposits.
  • Findings suggest potential for novel therapeutic strategies targeting CR1 in AD treatment.

Keywords:
Alzheimer’s diseaseCR1 densityCR1 length polymorphismcomplementcomplement C3b/C4b receptorcomplement receptor 1dementiagenetic riskmolecular biologyneurosciences

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