Related Experiment Video

Updated: Apr 18, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

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

Published on: July 18, 2017

12.4K

Plasma Complement factor H in Alzheimer's Disease

Michael A Williams1, David Haughton2, Michael Stevenson3

  • 1Centre for Medical Education, Queen's University of Belfast, Belfast, UK.

Journal of Alzheimer'S Disease : JAD
|January 16, 2015
PubMed

Insights

This study found that plasma levels of complement factor H (CFH) do not differ between Alzheimer's disease (AD) patients and healthy individuals. Therefore, CFH is unlikely to be a useful biomarker for diagnosing AD.

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) pathogenesis involves complement cascade dysregulation.
  • Complement factor H (CFH) regulates the complement cascade.
  • Previous studies on plasma CFH in AD have yielded conflicting results.

Purpose of the Study:

  • To investigate plasma complement factor H (CFH) levels as a potential biomarker for Alzheimer's disease (AD).

Main Methods:

  • Compared plasma CFH levels in 317 AD cases and 254 controls.
  • Utilized an immunodiffusion assay for quantification.
  • The study was powered to detect a difference of 23 mg/L with 80% power.

Main Results:

  • No significant difference was observed in plasma CFH levels between AD cases and controls.
  • The study lacked the statistical power to detect smaller differences.

Conclusions:

  • Plasma complement factor H (CFH) is not a suitable biomarker for Alzheimer's disease (AD).
  • Further research may explore other complement system components or biomarkers.

Keywords:
Alzheimer's diseasebiological markerscomplement factor H

More Related Videos

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

37.6K
Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy06:27

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy

Published on: November 30, 2018

9.9K

Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
1
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
2
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
2.0K
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
1
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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...
1.3K
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
13.2K