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Peripheral complement interactions with amyloid β peptide in Alzheimer's disease: Polymorphisms, structure, and
Jenny U Johansson1, William D Brubaker1, Harold Javitz2
1Biosciences Division, SRI International, Menlo Park, CA, USA.
Summary
Single nucleotide polymorphisms (SNPs) in the complement receptor 1 (CR1) gene are linked to Alzheimer's disease (AD) risk. This study found CR1 deficiency in AD erythrocytes, suggesting erythrocyte CR1 function influences AD risk.
Area of Science:
- Neuroscience
- Genetics
- Immunology
Background:
- Genome-wide association studies link complement receptor 1 (CR1) gene single nucleotide polymorphisms (SNPs) to Alzheimer's disease (AD) risk.
- CR1's presence and function in the human brain remain poorly understood, despite its abundance in erythrocytes.
Purpose of the Study:
- To investigate the expression and function of CR1 in the human brain and erythrocytes in relation to Alzheimer's disease.
Main Methods:
- Utilized Western blots, quantitative polymerase chain reaction, and brain immunohistochemistry.
- Assessed erythrocyte CR1 levels and CR1-mediated capture of amyloid-beta peptide in AD patients.
Main Results:
- CR1 was not detected in the human brain parenchyma but found in vasculature.
- Erythrocyte CR1 was significantly deficient in AD patients.
- Reduced erythrocyte CR1 correlated with increased AD risk, while increased erythrocyte CR1 correlated with decreased risk.
Conclusions:
- CR1 polymorphisms associated with AD risk likely exert their effects through modulation of erythrocyte CR1 levels and function.
- Erythrocyte CR1's role in capturing circulating amyloid-beta peptide may be a key mechanism linking CR1 to AD pathogenesis.
Keywords:
Amyloid β peptideCR1ClearanceComplement C3b/C4b receptor 1Complement receptor 1ErythrocyteImmune adherenceRed blood cellSingle nucleotide polymorphismMore Related Videos
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