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Related Concept Videos

Complement System01:27

Complement System

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Alzheimer's Disease: Overview01:26

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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Related Experiment Video

Updated: Jul 22, 2025

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
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High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

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Alzheimer's disease-associated complement gene variants influence plasma complement protein levels.

Aurora Veteleanu1, Joshua Stevenson-Hoare2, Samuel Keat1

  • 1UK Dementia Research Institute Cardiff, School of Medicine, Cardiff University, Hadyn Ellis Building, Maindy Road, Cardiff, CF24 4HQ, UK.

Journal of Neuroinflammation
|July 21, 2023
PubMed
Summary

Alzheimer's disease is linked to immune system changes. Specific gene variants in complement genes like CR1, C1S, and CFH influence protein levels, potentially affecting Alzheimer's disease risk.

Keywords:
Alzheimer’s diseaseBiomarkersC1qC1sClusterinComplement receptor 1Complement systemFactor HGWAS

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Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration
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Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration

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Area of Science:

  • Neuroimmunology
  • Genetics
  • Biomarker Discovery

Background:

  • Alzheimer's disease (AD) is associated with immune dysregulation.
  • Genome-wide association studies (GWAS) identified complement-related genes, including clusterin (CLU) and complement receptor 1 (CR1), as key players in AD pathology.
  • Complement proteins are proposed as potential AD biomarkers.

Purpose of the Study:

  • To investigate the relationship between plasma complement protein levels in AD and AD-associated complement gene variants.
  • To assess the predictive utility of complement biomarkers for AD diagnosis.
  • To identify novel associations between genetic variants and plasma complement protein levels.

Main Methods:

  • Plasma levels of clusterin, C1q, C1s, CR1, and factor H were measured in early-onset AD (EOAD), late-onset AD (LOAD), and control cohorts.
  • Receiver operating characteristic (ROC) analyses were used to evaluate biomarker predictive performance.
  • Genotyping data and GWAS were employed to assess the impact of single nucleotide polymorphisms (SNPs) on protein concentrations and identify new associations.

Main Results:

  • Plasma clusterin and C1q levels were significantly increased in AD patients compared to controls.
  • Plasma soluble CR1 (sCR1) and factor H levels were significantly reduced in AD patients.
  • C1q demonstrated the highest predictive value as a single complement biomarker for AD, with slight improvements when combined with other markers.
  • SNPs in CR1, C1S, and CFH significantly influenced the plasma levels of their corresponding proteins, while CLU SNPs did not affect clusterin levels.

Conclusions:

  • Complement system dysregulation is evident in Alzheimer's disease and may contribute to its pathology.
  • AD-associated SNPs in CR1, C1S, and CFH impact plasma protein levels, providing a potential mechanism linking these genetic variants to AD risk.